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Before
it’s too late - Katherine Nevius
(Printed in 'Boxer Quarterly' November 2003)
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 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 an 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 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 and six 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 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 there unsuspecting get. If you don’t test, you
don’t know your dog has thousands of VPC’s including the run 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 out 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 “Its 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 recognise that the boat in which finds
one-self is full of sailors, the loneliness of a sad secret is lifted. Even
in cases where breeders really believed there 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 half a
century ago by Frau Stockmann) began to make itself painfully known. And
once it was recognisable, 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 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 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 undoubtedly be to do it still I’d suggest you consider
falling on the sword – for the literal survival of this beautiful breed in
England.
Consider adopting the testing regime 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 have waited to 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 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, USA |
this horrible heart condition. 
The diagnosis that my vets
had already suspected was now confirmed: cardiomyopathy. I was warned that
the prognosis was poor: at best he might live for six months - or he could
die the following week.