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  • Writer's pictureKatherine Goliboski

Responsible breeding goes right to the heart.

Updated: Apr 4

Meet Venger (Cidwm’s Forsaken Avenger). She is called Venger as her mask was so dark as a newborn, it looks like the mask used by heroes like The Lone Ranger, so we took to calling her the Masked Avenger -- and it stuck. Especially when she would commit daring feats that scared us half to death (escape attempts, sleeping beneath her mother’s underarm…).

Venger is now 11 weeks old, and we love her dearly. She is brave, confident, smart, and active. She has a beautiful, delicate face.

You wouldn’t know she has a potentially fatal heart defect.

At 7 weeks old Venger was diagnosed with a grade III heart murmur (highest grade being VI). Heart murmurs are not common in our breeding program. Both her parents are heart clear, although her mother did have a grade I heart murmur at 7 weeks that had resolved by 11 weeks. Her father’s health is impervious, thankfully.

Venger’s diagnosis prompted a cardiologist referral and assessment. This resulted in a diagnosis of Patent Ductus Arteriosus (PDA). The short description of this defect is “an unclosed hole in the heart” (American Heart Association, 2020). The long answer is that the hole in the heart where blood circulates during fetal development to avoid the as-yet non functioning lungs, does not close (typically a result of first inhalations following birth). There can be secondary symptoms such as coughing, gasping, lethargy, loss of consciousness, faster or harder breathing than normal, and difficulties eating or growing at a normal rate.

The good news: Venger’s symptoms are limited to faster breathing/heart rate.

How does this happen? Apparently this is the most common congenital defect in dogs (Broaddus & Tillson, 2019) -- did you know that? We didn’t. PDA is described as “quasicontinuous, that is, a threshold trait with graded phenotypic expression. In other words, the chance of a dog having PDA and the severity of the abnormality increase with increasing amounts of defective genome from the parents” (Broaddus & Tillson, 2019). Problem is, our parents had no familial history with this defect in the last 15 years. However, as is the way with any type of animal breeding, you do not have conclusive information on ALL family members. Times and science changes, so what would now be an easily detectable problem now may not have been acknowledged before.

There is a very interesting study entitled Hereditary Patent Ductus Arteriosus and Its Sequelae in the Dog (written by Patterson, Pyle, Buchanan, Trautvetter, and Abt in 1971) looking into the inheritance of PDA specifically. They did a number of test breedings to investigate the inheritance, not only from those affected, but by siblings of those affected as well. Their study concluded that of course there was a high amount of heritability as a result of direct breeding of affected dogs, but also a high heritability when affected dogs were bred to siblings of other affected dogs. I must say that the biggest gap in this study was the lack of exploration of breeding siblings of the affected to non affected dogs. They also did not include neonatal deaths under 1 week old, which in our opinion should have been considered. We ourselves lost a sibling of Venger’s at 3 hrs post birth due to PDA. This event itself prompted initial research/exploration prior to Venger’s diagnosis - although due to the nature of the defect, one could not conclusively at that time rule is as a ‘defect’ as opposed to a time-sensitive lack of development (the hole that causes a PDA can take up to a week following birth to seal over as a normal development).

So what happens now? Well, as we are responsible breeders who care about all our puppies, we have scheduled an appointment with the Ontario Veterinary College for a surgical consult, and in turn been assured that within a month of this consult she will be able to have this defect surgically repaired. Following that, she will have a 100% normal life. This surgery may be done laparoscopically, or may be open-heart -- it depends on the severity of the damage done in the interim. Either way, we will do what needs doing and take care of her.

What does this mean for our breeding? Well, not that it really changes plans for the parents, as this was Acadia’s last litter regardless and likely Xach’s as well. Acadia is to be spayed and Xach… well James and I agree to disagree on that ;) Time will tell, but he will not be bred. It is interesting to us that this occurred as both parents have a very low inbreeding coefficient, and come from (as far as we know) sound outcrosses. Just goes to show genetics are never certain, merely genes in a blender -- you never know what will float to the top.

We were going to keep a female from this litter for future breeding -- due to the uncertainty of the genetics behind this particular defect we have decided against that. We are co-owning a male from this litter, and perhaps down the road he could be bred to an unrelated female with a clear heart familial history, but that is a long way away and requires more research. In the meantime we will enjoy pampering him alongside his other owner.

Venger may decide she wants to go to a different home following her recovery, we will broach that topic with her once the dust has settled. Until then, as we will forever, we love her.

Works Cited

Broaddus, K.D. and Tillson, D.M. Patent Ductus Arteriosus in Dogs . Cardiology Compendium. September 2010 (Vol 32, No 9).

Abt, D.A., Buchanan, J.W., Patterson, D.F., Pyle R.L., and Trautvetter E. Hereditary Patent Ductus Arteriosus and Its Sequelae in the Dog. Circulation Research. July 1971 (Vol. 29, No 1).

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