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This article was originally published in the UK Boxer Quarterly.  Ed.

In the United States and Canada, an inarguable case has been made: We have a problem, and it’s a big one. For the better part of a century, the Boxer, whose fanciers followed the dictates of a standard that made it possible to create this breed in the first place, has been inbred on traits that are phenotypically desirable. The trouble with fixing type in a breed is that one also runs the all-too-difficult-to-avoid risk of fixing undesirable genotype as well. This, breeders in North America appear to have done in spades where one genetic disease is concerned. It’s called by a number of names, but usually it’s known as Boxer Cardiomyopathy.

We got where we are because, more often than not, this disease presents with one symptom only: sudden death. In the past, if we were lucky, as an animal matured it might get through that asymptomatic stage and actually faint a time or two before the big event that ended its life. If they received this warning, they were able to relieve it of its breeding responsibilities. But mostly, they didn’t know that our Boxers had it. Thus, until they were presented with the option of a testing protocol only recently, breeders blithely and even ignorantly bred happily away, making sure that, over the decades, our dogs faced an uncertain future we’d never even imagined, much less intended.

The test we have available now isn’t fool-proof. But it is the only test we have. And although it cannot, yet, be said to clear any dog – it can most certainly condemn one. And therein lies the reason that we all must test.

Every board-certified cardiologist studying the Boxer here is unequivocal on this point: Before breeding, Boxers must undergo the rigors of the Holter monitor, a twenty-four hour electrocardiogram that presents evidence (when evidence exists) of the premature contractions of the ventricle that, when occurring in multiples of four, five, six and upward (ventricular tachycardia) can cause the sudden death of an otherwise healthy-appearing dog.

A couple of studies are currently ongoing in the United States to discover the mode of inheritance of this gene – a dominant one with variable penetrance, according to the study funded by the American Boxer Club being conducted at Ohio State University by Dr. Kate Meurs. She would be the first to tell you that there is no hard-and-fast rule that allows her to look at a Holter result and declare the fitness for breeding of every dog tested. But she’d also be the first to tell you that the test must be done in spite of the remaining aura of uncertainty where results are concerned.

In speaking with Dr. Meurs' assistant two days ago (as I sent in the first of four Holter tapes with which I was faced recently), I heard the theme played again:  Young Boxers in the study at OSU have been tested clear on a couple of yearly Holters, then suddenly evidence of BCM rears its ugly head.  The converse is true, as well:  She suggested that an adverse reading on a young dog should not be sufficient evidence upon which to base his or her removal from a breeding program.  One should hold off, and test in subsequent years to see what happens.  

This is because of the apparent variability of both symptoms and clinical signs -- and because of their odd relationship to each other. Here, we've all heard of the dog with hundreds of VPC's (confirmed to me by OSU) who never exhibits symptoms and lives to a ripe old age.  On the other hand, dogs clear on Holter can keel over dead.

So why do we do this test?  We do it, and I believe we must do it, for two reasons:

The first is that there is a certain percentage of severely affected dogs without symptoms who WILL keel over eventually – as will some of their unsuspecting get.  If you don't test, you don't know your dog has thousands of VPC's including the runs of ventricular tachycardia that kill.  Breed this dog at the rest of the Boxer-lover's world's peril.  

The second reason to test is simply to add to the increasing body of knowledge where this affliction's concerned.  If we don't test and share our results, we will never find an answer, if an answer's available to be found.

I know that sometimes that last seems questionable.  Researchers become increasingly vague about what dog is breeding material and what dog is not. But testing is the only way we'll ever find a road out of this mire, if there is such a road.

When I started in Boxers over a decade ago, old-time Boxer breeders were in denial. Rumors were rampant because enough unexplained early deaths had occurred to be definitively noticeable. But "It’s not in my line" was the mantra of the era. Fingers pointed in every direction attempting to shift suspicion elsewhere.

Then the age of the Internet arrived, and as novices like me entered the scene – folks who had no ways in which to be set and were, thus, less likely to dig in their heels and deny – eventually open discussion began to make clear the breadth of this problem, and even many experienced breeders came around, no longer having to feel so alone or maligned. After all, once you recognize that the boat in which one finds oneself is full of sailors, the loneliness of a sad secret is lifted. Even in cases where breeders really believed their dogs had probably succumbed to allergic reaction to bee sting or any other such explanation, clarity flooded the pages of mailing lists; we all discovered reality and, once reality was clear to the leaders of the American Boxer Club, funding began to pour forth in hopes that the mysteries of this unfortunate genetic defect could be explained.

Here in North America, the horse is long out of the barn. We had no wisdom to guide us when first our breed’s predilection for unexplainable early mortality (documented even a half a century ago by Frau Stockmann) began to make itself painfully known. And once it was recognizable, the occasional naysayer still refused to see this particular forest for its trees. Given recent events in the United Kingdom, it appears that some breeders there are poised, themselves, to venture down that same lamentable road. Only doing so is so totally unnecessary -- because others have been there before you and blazed a clear and crucial trail. You have only to follow it.

If you suspect that the gene for Boxer Cardiomyopathy may exist in your present breeding stock, it may not be too late to benefit from the mistakes North American breeders made so long ago. If it is indeed concentrated in only a few places at present, and you know in your own heart that the hearts of some of your line’s best may be affected, difficult as it will undoubtedly be to do it still I’d suggest you consider falling on your sword -- for the literal survival of this beautiful breed in England.

Consider adopting the testing regimen we’ve been so clearly exhorted to follow here, or at least remove from your breeding program any dog you suspect may be implicated until you CAN test. Don’t wait until you’re where we here in the States and Canada are – coming to the conclusion that, given the inbreeding that’s been done for decades on this unfortunate trait, it’s possible that we may just have nowhere on this continent left to go.

Some here still pin their hopes on the eventual discovery of a genetic marker. In so doing, I fear they may find that they may have waited too long -- that the marker will discover only that all of our dogs carry the gene. It truly appears to be pandemic here. It may not ever have to be where you are.

The saying goes that when God closes a door, somewhere He opens a window. In the UK, there may exist a small window of opportunity in which to do the right thing. I wish for you the wisdom, and the generosity of spirit, to do it before the window slams tightly shut.

Katherine Nevius
Minstrel Boxers
Vienna, Virginia

USA