THIS IS THE FACE OF BLOAT by Kate Connick

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Editor's note: My thanks to Boxer owner extraordinaire Kate Connick for sharing this "bloat early warning system" with those of us who have never experienced the condition in the dogs we live with. And for providing the best home for one of my puppies this breeder could ever have hoped for.

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Yes, Tonka experienced GDV (gastric dilatation and volvulus, aka bloat/torsion) on Tuesday. This isn't an uncommon disorder, and I'm sure some of you have experience with it. My very first exposure was watching a neighbor's great Dane die this way when I was a kid. Horrible way to die, I might add.  But some of you haven't had firsthand experience with bloat, so I figure I'll share Tonka's tale to make it real for you. If you aren't already familiar with GDV, you want to know about it - whatever kind of dog you have. This is potentially one of the ugliest, most urgent and lethal situations that you may face as a dog owner, and you don't want to be farting around online asking people what they think about your dog's retching and pacing as he slowly dies in front of you. Take a few minutes to learn so that you're prepared.

An excellent article about bloat can be found here: https://www.akcchf.org/canine-health/top-health-concerns/bloat/understanding-bloat.html#Warning

Tonka belongs to several of the high risk categories: He's a large, deep chested, male boxer with a temperament that is excitable and anxiety-prone. His 9th birthday arrives before the end of the month, and age is a significant risk factor. They don't know exactly why that's so, but it may be that ligaments become more lax, or other health conditions like tumors may serve as contributing factors. Whatever the reason, bloat risk increases with age.

Tonka leads a sensibly bloat-preventive life. He doesn't exercise before or after meals, doesn't eat large meals, and isn't fed when he's panting. He has a varied diet, eats multiple small meals daily, doesn't gorge his food, and generally doesn't overindulge at the water bowl. He's lean but fit and overtly healthy.

Even though he has ARVC ("boxer cardiomyopathy") and a cardiologist told me, years ago, that he was "at high risk for sudden death, with or without medication," he has led a full, active life. He hikes, swims, runs, plays, and you'd never know he was a cardiac patient if I didn't tell you. But he is - and this is relevant. Since his ARVC diagnosis when he was a year and a half or so old, he's been sedated and locally anesthetized for a few, relatively minor procedures, but he hasn't undergone general anesthesia. Too risky.

There was absolutely nothing unique about the day he bloated. It was a typical day. He had hiked the day before, and the morning of, he went swimming with his "siblings." He retrieved, swam with me, and rode on a float - but his exertion level wasn't unusual, and he didn't have an unusual amount of treats or drinking water. It was a typical day.

My first sense that something was amiss was on the car ride home. He usually sleeps, but he was restless - and this is unusual for him. Anyone who has ever ridden in my car knows that I keep it cold enough to induce hypothermia in a polar bear, but Tonka was panting. He would lie down, then get up - panting - and look out the window. I'm not a worrier, so my assumption was that he probably had to go to the bathroom. Still, I must have had some sense of foreboding; I kept an eye on him in the rear view mirror as a drove. He did settle, but not as restfully as usual, and he would alternate rest with standing and panting. Why didn't I just pull over and give him a chance to go to the bathroom, you ask? Oddly, that's what I would have done any other day. My thought bubble was telling me I should just pull over, yet I felt a bit of urgency to just get him home.

It's an hour drive. Once home, it's another half hour to unload the car and put stuff away. The dogs were in the backyard or house - kind of following me around. Tonka's behavior didn't seem particularly unusual at that time.

Then I sat down with my sister to chat, and that's when I grew increasingly concerned. Know your dog. Know what's normal and what isn't. And pay attention to it. All of Tonka's symptoms were relatively subtle, but I found myself staring at him. I wasn't even consciously thinking. I was just staring at him with a pit in my own gut, until I said, "I think he may be bloating."

What were his symptoms?

* Panting. Yes, it's a summer day, but I keep my house cold. The dog should not have been panting. It was more of a pressured panting, the kind prompted by stress or pain.

* Comfort Seeking. Yes, he's an affectionate dog, but he'll typically flop on a dog bed and snooze when we get home. He persistently stood next to me, basically in heel position beside my chair, and solicited contact. Sometimes dogs aren't flattering you but are trying to ask you for help.

* Restlessness. Again, his typical behavior would be to just lie down and relax. He wanted to. He'd approach a bed or the sofa, maybe dig a little like dogs do before they lie down, and then abandon his effort to return to my side.

* Posture. His back was slightly arched, just enough to look slightly uncomfortable.

* Tight abdomen. His belly felt very tense to me.

* Inability to vomit? A couple of times, he dropped his head and bee-lined away, in the way a dog might as it's preparing to vomit - but then he simply didn't, and he returned to my side.

Mostly, he just appeared to be panting, restless and clingy - and this is not typical behavior for him, but it also wasn't overwhelmingly obtrusive. If the house wasn't air conditioned, if there were other activities going on where his restlessness and neediness weren't so apparent, would his dilemma go unnoticed? It can happen. Bloat can happen very quickly, often at night, and it's easy to not realize what's happening until things are more advanced. There were some characteristic symptoms that he didn't display. He never physically tried to vomit; there was no retching, dry heaves, or anything like that. His belly wasn't swollen; it simply felt extra-firm to the touch. His color was good. He wasn't having any mobility issues (jumping into the car, for example). He's stoic, so you could squeeze his belly like a python might, and not get any reaction.

Off to the vet we went. I walked in to my vet's office, was greeted by a staff member who knows me well, and when I quietly said, "I think Tonka may be bloating," they mobilized like a tornado. I'm not a very dramatic individual, so I did have a passing thought that I was going to feel like a first-rate jackass if the dog just had a stomachache or a pinched nerve. That said, sometimes you don't want to be right, and I didn't want to be right about the whole bloat thing. Being a jackass isn't always a bad thing.

The vet immediately looked at him. Abdomen didn't seem particularly tense to her (again, know your dog - for him, it wasn't normal). Heart rate was normal. Color good. She almost looked relieved, but obviously they took xrays right away - and while he wasn't dramatically bloated, he had torsed. In simple terms, his stomach got acrobatic and did a little somersault so that it was cutting off circulation to itself and everything beyond. And that's a B.F.D. This is one of those genuine, life or death situations!!!

My options:

Option 1. Euthanasia. That sounds horrific to even consider, but we're talking about a nearly 9 year old boxer with a serious heart condition (who might not even survive anesthesia itself, much less any of the nastier side effects that GDV can bring, like heart arrhythmias, sepsis, organ damage/failure, etc.). This is something people often opt for, out of concern for their animal's comfort and/or an inability to justify the financial burden of more intensive intervention. Resist the temptation to pass judgment on anyone who feels that this is the most sensible decision. Sometimes it's a kindness to spare a dog from the prolonged discomfort of hopeless surgery and aftercare. Seriously, don't judge people who make different choices than you. We all do the best we can for the pets we love, given our knowledge and resources at the time. Be kind.

Option 2. A tricky, difficult, and expensive surgery with no real guarantee of success. These surgeries and the aftercare are very, very expensive - and no, not because veterinarians are thieving villains but because the surgeries aren't easy. The interrupted blood flow can wreak all sorts of damage, and to be honest, my vet's practice isn't particularly equipped to do this sort of surgery. It's more of an emergency-vet thing, but it's also a time-is-of-the-essence thing, and he was already at my vet's - and I was insistent that he have surgery in familiar surroundings, under the care of people I know and trust. Not to be grim, but if he was going to die, I wanted it to be in more comforting surroundings. He's a high anxiety type of dog, and especially with the aftercare, it was important to me that he be attended to by friends and not strangers.

So yes, I went for Option 2. Tonka has been active, happy, and sometimes you just have the subjective sense that the dog isn't ready to die. And no, I don't have health insurance for this dog, but that's okay. I kinda like the old guy, so I'll deal with it. My vet protested and really wanted me to consider taking him to an emergency center for surgery performed by specialists who do this sort of thing frequently, but she understood my reasoning for wanting her to do the job, and she rose to the occasion. Heroically, I might add. I don't think either of us was necessarily optimistic about what she'd find once she cut him open, but apparently I'd gotten him there quickly enough, and they started him on fluids and painkillers right away. In terms of a rough timeline, his bloat symptoms started around 1pm; I had him at the vet by 3:30 or so, and he was being cut by 5-ish.

He was in surgery quickly, and the worst of it was the torsion itself. He wasn't terribly bloated. His organs and blood vessels appeared healthy, so she didn't have to remove necrosed tissue. His spleen looked just fine, as did the stomach and intestines. These are good things. His heart held up astonishingly well throughout surgery. Go figure. His stomach was re-positioned the way it's supposed to be, anchored in place, and he was stitched back up. That's only the first hurdle to recovery.

I visited afterwards, and he was stoned off his gourd. Visited the next day (Wednesday), got him to drink a little water, eat a little food, and pass some stool while taking a little walk. He was still pretty dopey from drugs and fatigue, but they let me hang out on the floor with him in an exam room while he napped.

Pro Tip: Send pizza to the vet office. They like treats just as much as dogs do, and with rare exceptions (I hear you, gluten intolerants), who doesn't enjoy pizza? They genuinely saved this dog from certain death. GDV is that sort of situation.

Realistically, part of this process is understanding that you can only control so much. I did my job by getting him to the vet quickly. She did her job by doing her thing quickly and competently. His body seems to be doing its job, but that's always the wild card. Some dogs just suffer too much damage - and well, he IS an older dog with a defective heart who probably shouldn't even be alive anyway! (Note of hope to those with ARVC-afflicted dogs: The medications can be absolutely amazing in giving these dogs genuinely full lives).

Tonka has been eating, resting, gaining alertness, and he continues to look stable and well. The vet is continuing to adjust medications to finesse his treatment, and she'll recheck his bloodwork later, but I'm hopeful he'll be able to come home soon. If this dog manages to get through this and celebrate his 9th birthday on the 27th, it'll be a minor miracle. Amusingly, his breeder had asked me to choose an Eagles song for his registered name (that was the theme for the litter). As much as I like the song Desperado, I just couldn't name my dog that. So I opted for the song Take it to the Limit. I have a friend who believes that dogs become their names. Maybe there's something to that.

Saturday follow up:  Tonka was able to go home Thursday evening.  He had some issues with reflux, but with medications and many small meals throughout the day, that appears to be under control.  He lost about 6 pounds, but he's ravenously hungry and eager to regain it all.  Astonishingly, his bloodwork was normal throughout this (with the exception of an increase in WBCs), and he is off all painkillers - but other than being tired, he appears to feel pretty good. 

A Brief Journey through the American Healthcare System...via Medicare (Copyright 2020 Virginia Zurflieh)

 

Author’s note: I’ve published this account on my Boxer Underground Blog, but be forewarned, its only relation to Boxers is the fact that my son and daughter moved in and cared for my three Boxers (and me) while I was in the hospital, and later, while I was recovering at home. Thanks, Linda and Rob! (Photos of Uno, Emma and Remy by Robert Zurflieh)

 

A Brief Journey through the American Healthcare System

…via Medicare

Copyright 2020 Virginia Zurflieh

 

What was I thinking? Apparently, that I was going to glide serenely through life from my 77^th birthday to my 100^th (thereby topping my mother’s record by 57 days) and arrive at a painless oblivion sometime thereafter…in my sleep.

I didn’t purchase a Medicare supplement and I hadn’t updated my six-year-old “homemade” will. I intended to have plenty of time to take care of things like that later.  I did sign up for the prescription coverage part of Medicare (Part D) – which is basically private, for-profit insurance – when I retired 12 years ago, but dropped it shortly thereafter. The insurance provider had steadily increased their rates, despite that from that date in 2008 to the Saturday morning in 2019 on which I went to the hospital, I was filling only one $10 prescription a month, plus the odd antibiotic for a dental procedure or sore throat now and then.

Then…WHAM…a trip to an urgent care clinic early one Saturday morning, a CT scan, a trip by ambulance to the hospital, more CT scans, exploratory surgery and a 28-day stay in the hospital followed by a 20-day stay at a “rehab center” – really a nursing home and a truly awful place. Also, three subsequent week-long stays at the same hospital and three months of home healthcare.

In addition to learning how totally unprepared I was for a major medical emergency, I also gained some insight into several facets of the American healthcare system that I would never have been aware of if I hadn’t been personally confronted by them.

1.    Immigration (yes, immigration): Judging by the hospital I stayed in, immigrants are utterly essential to the for-profit American healthcare industry, especially in Florida. My first stay was 28 days on an ICU floor. A large percentage of both the professional and support staff were immigrants. Many, but by no means all, were Hispanic. My surgeon was Croatian; the cardiologist was Indian as is my primary care physician (PCP); the GI specialist was Middle Eastern. Everyone that I encountered was competent and courteous. Most spoke fluent English. The same was true in other areas of the hospital in which I stayed during subsequent admissions. I can’t imagine how this hospital could have functioned without its immigrant staff.

 

The staff at the “rehab center” at which I spent 20 miserable days was also largely comprised of immigrants, but although most of them were helpful and kind, some spoke almost no English and were clearly several rungs down the status ladder from their hospital counterparts.

 

2.    Pain Management (as opposed to pain relief): Because of the current opioid addiction crisis, doctors these days live in fear that their patients are going to become addicted to the pain medication they prescribe. So, they prescribe as little as possible for as short a time as possible.  For me, it was simply a matter of trying to time one of my steadily decreasing number of pain pills per day to a half hour before the wound-care nurse came to change the wound vac three times a week. For people with unbearable, long-term pain – cancer, a broken hip, a condition that cries out for heavy-duty opiates on a regular basis – the prospect of their physician’s new pain management protocol must be terrifying.**

 

3.   Physical Therapy: PT joke: “I’m a Personal Torture Instructor…I Mean Physical Therapist.”  I’m sure many people benefit from physical therapy – people who’ve had orthopedic surgery to repair or replace a knee or hip, for example.  But I wasn’t in the hospital for a hip replacement and attached as I was to IVs and other medical paraphernalia, wasn’t even up for a walk to the bathroom. Nevertheless, because physical therapy providers contract with hospitals, rehab centers, etc., for so many hours of PT per patient whose PCP has prescribed it (mine was a PT believer), and because they only get paid if they perform the stipulated number of hours of PT, I was confronted several times a day by a pair of chirpy, gung-ho twenty-somethings who were determined that I was going to get out of the bed where I had been trying to catch up on sleep (ironically, the hospital was not a very restful place) and do anything that counted as PT, even just sitting up in the chair beside the bed for 30 minutes; or when I finally got to a bathroom sink, helping my daughter help me wash my hair. Torture – no; constant annoyance – yes.

 

4.    Big Pharma, Big Medical Bills and the rest of the story:

Here again, my ignorance of the American healthcare industry showed. When I signed up for Medicare Part D again in November 2019 after I got home, I learned that although the cost would have been $87 a month for the Part D insurance had I signed up when I first enrolled in Medicare and kept paying the premiums, it was now going to be $87 plus a $40 a month penalty…for the rest of my life. In other words, the insurance company was going to get theirs one way or another. Nevertheless, because Part D lowered the cost of one of my prescriptions from over $500 for a 90 days’ supply to $135, and because I had (due to dumb luck/reasonably good health) avoided the cost of that insurance for over 12 years, I didn’t say a word.

 

Another thing I learned was that neither my family doctor nor the cardiologist who prescribed the expensive medication seemed to have any idea what prescription medicines cost these days. Because my new Part D prescription coverage didn’t go into effect till January 2020 and I couldn’t afford $500+ for the medicine the specialist insisted I take, my doctor persuaded him to provide me with free samples. Then my daughter spoke to his office manager and she gave me a coupon for a free 30 days’ supply, which tided me over till January. (Who knew there were coupons? Not the cardiologist, apparently.) The last time I tried to order a 90 days’ supply, the pharmacy clerk told me I’d reached a “coverage gap,” and 90 days’ worth was going to be well over $300 (the dread donut hole?). I was able to order 30 days’ of the medication for only $45, however, so I took it and will worry about the coverage gap when I run out again at the end of the month. 

 

That was just one example of the outrageous cost of many prescription drugs for which there are apparently no cheap generic equivalents…but which miraculously become affordable once one purchases the Part D insurance.

 

As for big medical bills, Medicare came to the rescue again. The hospital bill was nearly $34,000. Medicare paid over $32,000; my copay was $1364. Certainly not a small amount, but compared to $34,000, a pittance.

 

The bill for my surgery was $89,700. And keep in mind, the anesthesiologist, radiologist, and other medical groups involved with the surgery and hospitalization billed me separately. The surgical group sent an itemized bill, but looking back over it, I can’t figure out what Medicare paid and what Medicare disallowed, or “adjusted,” (a term used numerous times in the surgeons’ bill). In the end, however, if my copay – less than $500 – was 20% of the amount Medicare approved, Medicare staff obviously adjusted the charges down to a tiny fraction of the original amount billed. No wonder some doctors don’t want to accept Medicare patients. 

 

The Rest of the Story: When I began this account, I intended it as a paean to Medicare. Even after I put $10,000 in copays and related expenses on credit cards and ended up with a $240 monthly premium for Medicare Parts A, B and D (deducted every month from my Social Security check); and even after I realized that I would not be off the hook for private, for-profit insurance if I wanted to avoid bankruptcy on a government healthcare insurance program that I had paid into for 55 years, I’m still profoundly thankful that I was covered by Medicare. But every time I feel a little twinge in my side, I wonder how I’ll manage financially if I have to be hospitalized again (I won’t qualify for a supplement for two years, if then, and if I can afford it then); and I also wonder – considering the Covid-19 Pandemic – what is happening to the millions and millions of Americans who aren’t covered by Medicare.

** https://beta.washingtonpost.com/health/opioid-crackdown-forces-pain-patients-to-taper-off-drugs-they-say-they-need/2019/09/10/3920f220-c8da-11e9-a4f3-c081a126de70_story.html

  

Dr. Bruce Cattanach on Breeding from White Boxers

Editor’s note: This very timely piece is one of the last articles I received from Dr Cattanach, and was published in the May 2019 Boxer Digest along with some wonderful photos from his website of Dr Cattanach with Ch Steynmere Nightrider.

VZ

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When my ex-husband and I started out in Boxers in 1973, we quickly learned not to question (at least not openly) the American Boxer Club’s proscription against white Boxers: to wit, “reputable” breeders were not to register, sell or even “place” the white puppies that appeared with great frequency in flashy x flashy litters…despite that backyard breeders were free to sell “rare white boxers” for many times the price of a plain brindle puppy from a champion-sired litter. The rationale for that proscription was the alleged poor health and genetic inferiority that accompanied white coat color.

The ABC has come a long way since then, bowing to the lobbying of many of its members, especially new members, who wanted to be able to acknowledge their white puppies and place them in loving homes, along with the fawn and brindle “pet” puppies in their litters. The relatively new AKC Limited Registration policy greatly facilitated the ABC’s official enlightenment on the subject.

Now, some breeders are discussing the possibility of being able to use white boxers in their breeding programs. The following is a letter sent by UK geneticist and Boxer breeder Dr. Bruce Cattanach to a group of Italian Boxer fanciers,

VZ

29<sup>th</sup> March 2019

Breeding from white Boxers

Dr. Bruce M. Cattanach

Steynmere Boxers

I have been asked to comment, as a professional research geneticist and experienced UK Boxer breeder and judge, on the belief of some breeders that white Boxers are prone to health problems, and that breeding from them therefore poses risks to the genetic health of the breed.

 

My short answer is that there is no basis whatever for this idea.

 

The rationale for my response lies primarily with the fact that the white spotting gene responsible for the white ‘colouration’ in Boxers (s^w)  is the same as that for the white coats in dogs of a number of breeds (Bull Terriers, Sealyhams, Dalmatians etc) and in none of these breeds have serious abnormalities been found.  There is however a variably minor incidence of deafness in these white dogs, but this is well known and understood. 

The validity of the above statement is confirmed by studies at the DNA level which have shown the same gene locus is involved in these ‘white spotting’ breeds.  That there are other breeds, such as Collies and Dachshunds, which have dogs with white markings that ARE associated with serious abnormalities, is irrelevant, as the gene, Merle (M), responsible for white markings in these breeds, is different from that in Boxers (s^w).  M functions in a different way from s^w, it is located on a different chromosome, and also has a different mode of inheritance.  The white Boxer is not at risk of any defects other than, as said, the low risk of deafness.

How large is the risk of deafness? 

I know of no scientific study on deafness directly in Boxers.  A best guess for incidence of deafness would be that it will be similar to that in White Bull Terriers, a breed in which the incidence has been found to be less than 2%.  This is a breed in which, like Boxers, there has been no selective breeding for the presence/absence of pigmented patches in whites.  The incidence of deafness is higher in Dalmatians (5% to 12%) but this higher incidence has been attributed to the heavy selection for totally white dogs in this breed (excluding the spotting which derives from a different mechanism); pigmented patches are not wanted in Dalmatians, only spots. And deafness correlates with pigmentation seen in the coat.

It may help understanding of whites and deafness if the mechanisms involved are explained.  Basically, the primary effect of the responsible s^w gene involves pigment cell migration.  Before birth, pigment cells in the foetus are confined to paired sites along the back near the spine, from head to tail.  There may be three such sites on the head (around the eyes, the ears, and the occiput), perhaps six on the body, and several on the tail (numbers are based on my own studies).  Pigmentation, as we observe it, is achieved by migration of the pigment cells from their starting sites to spread down the sides of the body with most of the migration ceasing prior to birth.  It often incomplete such that more distant regions (between the eyes, and on the chest, neck, belly and lower legs) may not be reached and therefore remain white.  The ending of this migration is best seen on the head where it continues for several days after birth (the white blaze gets smaller and the nose becomes pigmented).  The pigment cells also spread internally where they give colour to the eyes and have a role in the maintenance of the auditory hair cells of the inner ear.  If they do not reach the eyes, the eyes are blue rather than brown.  If they do not reach the ears, the auditory hair cells die within a few weeks of birth, when hearing is then lost (about 6 weeks).  The migration is not uniform; left and right forelegs, for example, may have different amounts of white.  Likewise, the eyes can be of different colours (brown and blue) and, with the ears, deafness can affect one or both.  There is a correlation between extent of white in the coat and incidences of blue eyes and deafness.  This is best documented in Dalmatians: dogs with the most white in the coats are more likely to have blue eyes and become deaf.  The extent of the migration is loosely inherited.

As I have indicated, the white spotting gene (s^w) is primarily responsible for whites in Boxers but there are a number of versions (alleles) of this gene in other white marked breeds.  Only two of the versions now seem to exist in present-day Boxers:

-        the normal full-colour version (S) gives, in the double dose (S/S), solid Boxer which may still have a white chest spot and maybe white toes (the pigment cell migration is near complete).

-        the extreme version (s^w) gives, in the double dose (s^w/s^w), the near all-white dog, which may have occasional pigmented patches which are most often located around the eyes and/or ears on the head and more rarely elsewhere on the body. 

But the combination of the two versions (S and s^w) gives the intermediate, flashy Boxer that is generally favoured for show purposes. The white marking indicates the limitation of the spread of pigment cells.  In S/s^w dogs, the spread is less (more white) than in S/S dogs, and obviously far more than in near all-white s^w/s^w dogs.  Generally, the amount of white in the S/s^w dogs is less than one-third of the total, as actually required by the Breed Standard.

In summary, genetic studies indicate that white Boxers differ from flashy Boxers only by the more restricted level of pigment cell migration, and they are not at greater risk of major inherited disease that would validate their exclusion from breeding and showing.  They are, in any case, knowingly produced by the regular use of flashy animals for breeding.  Thus,

flashy x flashy produces  - 25% solid, 50% flashy and 25% white

But the Breed Standard does not disqualify the flashy white-producing dogs.  However, disqualifying whites from showing may be acceptable, but only for cosmetic reasons.   But to ban them for breeding based on imagined abnormality has no scientific justification.

If I may add my own view as a former Boxer breeder: I believe few serious breeders would want to produce high frequencies of whites, so matings of whites to flashy dogs would seldom be considered.  Likewise, matings between whites would also be avoided.  But if whites could be exclusively mated to solids, this could be seen as an acceptable breeding option and it would not ultimately cause any increase in the numbers of whites or damage the breed in any way.  Indeed, as all puppies (100%) from white x solid matings would be of the favoured flashy appearance, thus

white (s^w/s^w) x solid (S/S) can only produce flashy (S/s^w)

and these would breed exactly as flashy dogs from routine flashy x flashy matings.  It would leave open a further breeding option for show Boxer breeding. 

Added note.

I have bred from a number of white Boxers for experimental reasons, and always they bred exactly as expected, and none produced abnormalities of any kind. 

Bruce M Cattanach BSc  PhD  DSc FRS

(Retired as Acting Director of the Medical Research Council Mammalian Genetics Unit)

A Tribute to Dr. Bruce Cattanach

Dr. Bruce M. Cattanach

November 5, 1932 – April 8, 2020

Like many of my readers, the Boxer breed has been an all-consuming passion for most of my life. And the high point of my life in Boxers was flying to England in 1999 with my good friends Stephanie and David Abraham and meeting UK geneticist and Boxer breeder Dr. Bruce Cattanach at the Windsor Show. After Boxer judging, we drove with Bruce to see an early generation of his Bobtail Boxers and then followed him home to meet his wife Jo Peters (also a geneticist) and his own Steynmere Boxers.  

Dr. Bruce Cattanach was a brilliant man who made a huge contribution to the world of genetics (see the Harwell tribute below) and as at least a working knowledge of genetics became more and more necessary to the “art” of breeding dogs, was an invaluable resource to dog breeders in their efforts to avoid hereditary disease, especially in Bruce’s chosen breed, the Boxer. Throughout the following week, we will feature several articles written by Bruce on genetics for Boxer breeders.

VZ – April 11, 2020

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Medical Research Council Harwell Institute

Dr. Bruce Cattanach, former director of the MGU, has sadly passed away.

We are very sorry to announce that Dr Bruce Cattanach passed away on 8th of April 2020.

Dr Bruce Cattanach was an outstanding scientist who led the Mammalian Genetics Unit in its early years. Along with Mary Lyon, Bruce established Harwell as one of the great international centres for mouse genetics. He discovered the phenomenon of imprinting and was rightly considered a pioneer in this whole field. He also was a leading force in the field of dog breeding and dog genetics.  

He will be remembered as a gentle man who gave so much to all around him, family, friends and colleagues, with a wry sense of humour. He will be very much missed.

A Snapshot in Time

[Editor’s note: The piece below was written by Stephanie Abraham, the AKC Gazette Boxer breed columnist, for the July AKC Gazette. This breed column, “A Snapshot in Time,” was selected for republication in the next edition of the print and online AKC Breeder quarterly newsletter by the editor of the Gazette.]

      We live in an age of statistics in the dog world as well as the world at large. From crowd sizes at political rallies and sporting events to numbers of champions sired by a particular stud dog to size of entries under a particular judge—we can and do make judgments based on numbers.  

   However, it doesn’t hurt to point out now and again how these numbers may be skewed in a particular direction or altered over the decades based on new technologies or even changes in our national economy.

      Back in the day, when bitches had to be shipped by air and there was no AI breeding, stud dog statistics reflected those times.  In the 1970s, for example, shipping was the norm. I spent many an hour waiting or filling out written forms (no computers) at the cargo area at the airport. While Bang Away did sire 88 champions in the 1950s, the number of bitches sent to him was legion, and he remains #1 in AKC Boxer champions sired today.  This is a tremendous achievement, because of the sheer difficulty of physically getting the bitches to him, and the fact that he was only available during his actual lifetime—which in his case was relatively short--just under 8 years (Jan. 1949 - Feb. 1957). We can all argue with the benefit of hindsight about the good and bad contributions he may have made as our first real example of the ‘popular sire syndrome” in the breed, but the fact remains that his influence was indisputable.

     Today, freezing semen is commonplace. Dogs can and do sire offspring decades after their demise. We can ship chilled semen literally around the world using sophisticated extenders. So while production records may be eclipsed due to technology, we must remember that not all animals are being counted on equal playing fields. We reap the rewards today of advances in veterinary science and research, treating conditions that might have rendered animals barren not so many years ago. Times have certainly changed. The dog that sired 20 champions in 1960 might sire 40 or more today. 

     The advent of DNA analysis has made a dramatic difference in the dog world. Now we can test for health conditions, use more than one sire in a litter, and track generations to be sure of accurate records. Making breeding choices based on DNA analysis has arguably changed the entire world of purebred dog breeding. 

     Likewise, dog show numbers and judging opportunities have increased exponentially over the years. Hardly a weekend goes by without shows being available at increasingly closer distances. At the same time, entry fees have increased and travel is also more expensive. We constantly hear "too many shows, not enough good judges." While it is not in the scope of this column to argue that theory, it is clear that entry numbers have decreased and requirements for Majors in many breeds, and certainly Boxers, have decreased. In my Zone 1, Major requirements in 2018 have slipped to 9 and 14. I remember when Majors were 24 and 27, with far fewer opportunities to find them. Boxers were almost at the top of the list of all breeds when it came to Majors. How times have changed--and not just for Boxers but for many other breeds whose registrations have decreased even tho their popularity ranking has stayed relatively constant. Boxers have been in the Top 10 by popularity for a number of years lately. They were #3 during the Bang Away era. 

     So--- we need to be aware of all that has gone before us that has altered the way we look at our beloved breed. Numbers are just that--merely numbers that reflect on a particular point in history. One stud dog or brood bitch record is not "better" than another; it just reflects a snapshot in Time.  

Stephanie Abraham

Landmarks.properties@snet.net

Scotland, CT 06264

How to Win Friends and Influence Boxer People…NOT!

It’s 2018. Boxer entries are down all across the US, the new AKC point schedule shows our breed in decline and the AKC just announced that the German Shorthaired Pointer made it onto the top 10 most popular dogs list in 2017, knocking out the Boxer, who had been in that group for the past four years. In the same vein, ABC membership continues to fall and the print-your-own-ballot scheme that the board came up with not too long ago in an attempt to save money has had the unintended consequence of ensuring that only a fraction of the membership votes. In addition to all that bad news, ABC member clubs are also losing members and more of them are falling by the wayside every year.

So why did the ABC leadership choose this inauspicious moment in time to take a simple problem – the judge elected to officiate at the Maryland Regional had to withdraw due to illness, and the judge who came in second in the election had already accepted another assignment – and turn it into a crisis?

When the ABC was notified that the original judge had to withdraw, the president could have called a special meeting of the full board and asked for a consensus on a new judge from the directors, who are after all elected to conduct ABC business. Instead, a couple of officers unthinkingly appointed a judge who had just judged one of the pre-ABC shows in May 2017.

Naturally the Regional show chair, Tom Davis, objected to the ABC’s hasty choice, which he felt would hurt the entry at a show that Maryland Boxer Club members had worked long and hard to make a success. So he called the Salisbury KC show chair and suggested a popular breeder judge who had previously judged the ABC Futurity (and was also an ABC director) and the Salisbury Kennel Club hired her.

But because Tom Davis refused to accept the ill-considered decision of the officers who originally selected the new judge and acted on his own to solve what he saw as a problem the ABC was only making worse, a majority of the board voted to expel him from the ABC; because Bridget Brown, the breeder judge hired by the Salisbury KC, refused to withdraw from the Regional assignment, a majority of the board voted to remove her from the board by suspending her for six months; and finally, despite that the other members of the Maryland Boxer Club had done nothing wrong and had put on a great show, a majority of the board voted to sanction MBC for a year, during which time the club cannot put on an independent specialty show or even a designated specialty. Which brings me to the point of this blog:

Both sides made mistakes here, starting with the ABC officers who selected a judge who had just judged during the 2017 ABC week, in contravention of the spirit of the ABC’s own judges’ selection rules. But only one side was punished, and by any measure, punished out of all proportion to their actions. Expulsion?  A six months suspension?  A year’s sanction? And most of those actions were taken in the secrecy of an “executive session” of the board.

It’s 2018. Our votes for a new ABC Board of Directors are due to the teller by April 30. I have served as both an elected member of the board and as a zone director – I know how the board is supposed to act and it seems plain to me that the actions of most of the current directors in this instance were “prejudicial to the best interests of the club and the breed.”

If you agree, read the candidate questionnaires carefully and elect a slate of new members to the ABC BOD. It’s time to change with the times.

Thanks for listening.

A 2017 Update on JKD & ARVC Research

This update was originally published in the 2017 ABC issue of The Boxer Daily. It has been lightly edited. However, before you read about the progress that’s being made to find a solution to JKD (and ARVC), I’d like to direct you to www.boxerjkd.com. This website was created by a group of six Boxer fanciers, including three professional geneticists and several longtime breeders/exhibitors, to provide advice to Boxer breeders on how best to avoid producing Juvenile Kidney Disease – a devastating and inevitably fatal genetic illness – and to offer practical help and advice to the owners of JKD-affected puppies and adults.

Because there is not yet a gene test for JKD, the consensus of the three geneticists in our informal JKD group is that currently the ONLY way to stack the odds of not producing JKD in our favor is to avoid close breeding at all costs, and to eliminate from our breeding programs dogs and bitches that have produced an affected puppy. To that end, there are a number of pedigree programs that will help us avoid breeding two closely related dogs; and boxerjkd.com  has compiled a group of pedigrees from various parts of the world that identify dogs and bitches that have produced offspring that were diagnosed with JKD. (These pedigrees will soon be available on the boxerjkd.com Facebook page, too.)

It seems to be human nature to try to deny that a big health problem exists until it’s become an overwhelming problem. That’s what’s happened in the UK with JKD, and in the US with ARVC (we have JKD here in NA, too, but not yet to the same extent). For many Boxer fanciers, our whole lives revolve around our dogs. If you’ve ever lived with a JKD-affected Boxer, you’ll know that avoiding inbreeding and passing on the stud dogs and brood bitches that have produced offspring diagnosed with JKD is the very least we can do for our wonderful breed until a gene test is available.

VZ

A 2017 Update on JKD & ARVC Research

By Virginia Zurflieh, Scarborough Boxers

The Boxer community is a pretty tight-knit group of people, especially the breeders/owners/exhibitors in the English-speaking part of the world. And these days, most serious breeders have made themselves conversant with basic genetics as it applies to breeding Boxers. Our newfound familiarity with terms like “recessive,” “dominant,” “chromosomes” and “alleles” is due to a large extent to the persistence of British geneticist and Boxer breeder Dr. Bruce Cattanach in searching for a solution to various canine hereditary diseases, of which Boxers suffer more than their fair share. In fact, some genetic diseases and conditions, like ARVC and JKD, are forms of heart and kidney disease that afflict only Boxers.

Although already well-known to breeders in the UK and Europe, Dr Cattanach has most recently become familiar to Americans and Canadians by seeking out researchers working on studies that are aimed at eliminating those two often fatal “Boxer” diseases and persuading Boxer lovers to participate in the research via social media like Facebook.

One of these studies, on both JKD and ARVC, is ongoing at Cambridge University in the UK, where Professor Bill Amos is using new techniques to try to identify markers for JKD and ARVC. He is working with DNA from c.1000 Boxers, 100+ of them from the US and Canada. Prof Amos is still accepting DNA samples from Boxers that have been diagnosed with ARVC or JKD (called JRD or Juvenile Renal Dysplasia in the US). When I contacted him a week ago to ask if he wanted DNA from two recently diagnosed JKD cases of which I had just been made aware, he replied, “Definitely! Every case is desperately sad but worth its weight in gold.” So if you are unfortunate enough to own a puppy diagnosed with JKD/JRD or a Boxer diagnosed with ARVC and you wish to participate in Prof. Amos’ study, just email me at vzboxers@gmail.com and I’ll see that you get supplies and instructions and will send the completed kits to Prof. Amos at Cambridge. As always, the names of dogs and owners are held in strict confidence.

A second study, on ARVC, is being conducted by pediatric cardiologist & researcher 

Dr Robert Hamilton at the Hospital for Sick Children in Toronto. Dr Cattanach had previously collaborated with Dr Hamilton on an ARVC study that resulted in a co-authored journal paper that provided evidence that striatin, the gene identified by Dr Kate Meurs, was NOT the gene responsible for ARVC. But in the current ARVC study, Dr Hamilton, in Dr Cattanach’s words,”…has made a finding that I consider a breakthrough for Boxer breeders. It is what one might call a biochemical test for developing ARVC with the potential of recognizing the disease BEFORE clinical symptoms appear.” “This is not a gene test but should serve breeders well as a simple diagnostic test for the disease.” From Bruce Cattanach’s lips to God’s ears.

Previously, only one American dog in Professor Amos’ study had been diagnosed with JKD, but several were being treated for ARVC. It was relatively simple to put the owners of the ARVC-affected Boxers in touch with Dr Hamilton, whose staff then sent them blood/serum collection and shipping supplies. Dr Hamilton has paused his study while he publishes a paper and seeks funding to expand it, but I’ll continue to post updates on both research projects as I receive them.

At this point, I’d like to express my thanks to the many dedicated Boxer owners who participated with their Boxers in this research. I’ve been coordinating the submission of DNA swabs from the US & Canada to Professor Amos for over a year now, and have seen the dramatic response firsthand, with several owners submitting DNA for 7 or 8 dogs. 

Kudos, US & Canadian Boxer people – you’re the best!