Our Experience with Alopecia X or BSD

We have been involved with Pomeranians for approximately 40 years. When we started, we visited several famous breeders and were surprised that many of the dogs we admired were not shown to us. We learned later that it was because many of the adult males had lost their coats due to a condition in this breed known as Alopecia X, or BSD. As we got to know these breeders better and had demonstrated we could be trusted, we were shown these dogs and taken into the breeder;s confidence. This problem was absolutely NOT discussed publicly, in fact we were told if we did discuss it, we would be black listed and it would be assumed we had the problem. But we were determined that nothing can be fixed if it is just left alone, so we started asking questions – not pointing fingers, just asking questions, sitting quietly while various Top breeders discussed their experiences and discussed their own dogs and their theories on BSD.

We started our own breeding program with a normal coated son of Ch. Millamor’s Moon Rock, who was also in full coat till the day he died. Medallion produced many outstanding dogs that became top winners and producers. Unfortunately several of these offspring were affected with BSD. These included two BIS winning bitches Ch. Chriscendo Coy Coquette and Ch Chriscendo Carlotta. Although Carlotta did have a litter before she became affected, both of these bitches were put in pet homes. We had another BIS Medallion daughter, Ch Chriscendo Cover Girl, owned by the late Ed Jenner, who became affected after her show career was over and remained with Mr. Jenner as a pet for the rest of her life. We also acquired another Moon Rock daughter,  a BIS winner, who became affected and was placed in a pet home.

There were many outstanding dogs produced by Medallion throughout his lifetime that were normal coated; two of the most famous were Ch. Chriscendo Causin' A Commotion and Ch. Chriscendo Calvin Klein.

From the beginning, we were fortunate to have earned the trust of other breeders who allowed us to work with them and borrow their stud dogs. It was one of these instances that produced Ch. Chriscendo City Lights. As a young dog he was sold on co-ownership to the US and he did come back briefly to be used at stud. Sadly, he also became affected with BSD later in life.

We were very fortunate to work with the late Skip Piazza who lent us Ch Great Elms Firestarter, a full brother to Great Elms Prince Charming. Firestarter may have given us other issues we would have to deal with later but he produced two girls for us, both normal coated, Ch. Chriscendo Classica and Ch. Razzle Dazzle Classique, Classica, who was bred to the stunning young dog Ch. Chriscendo Centre Stage, a Calvin son and possibly the best dog we have ever bred. This breeding produced Ch. Chriscendo Classico, who was normal coated. Unfortunately Centre Stage was affected and when we realized that we never used him again.

Many of the pedigree's today feature Calvin and Classico and together they stamped the look we were trying to achieve and have become well known for.

We admired a young dog, Ch Starfire's El Hottie who was normal coated when we saw him and who we felt would be would be an outcross for us. The resulting breeding produced two outstanding puppies. The bitch, Ch. Chriscendo Chili Pepper, a very normal coated BIS winner and her lovely brother Ch. Chriscendo Coldplay who was not so lucky; and he was removed from our breeding program. We recently found out from his breeders that Hottie was affected.

More recently, Ch. Chriscendo Call To Arms, who has become an excellent producer for us and many other breeders, is in lovely coat today at 11 years old but like many of the top stud dogs today has produced, on occasion, affected offspring. We have kept, as has always been our policy, normal coated daughters and they in turn have been bred to several outside dogs. Our policy has been to only breed to normal coated dogs. We can do nothing about not being given the information when we breed to outside stud dogs, or breeding to a dog that later becomes affected. We too have not only been betrayed but lied to, and about, by others in an attempt to hide the facts. No one is exempt!

In an effort to lessen the problem of BSD we continue to work with other like-minded breeders and use normal coated dogs from around the globe. Most are from within the same family of dogs as we feel complete out crossing would be counterproductive. We acquired a young, normal coated dog, Ch. Silhouette Say It Right who is producing quality offspring. We also continue to buy and lease bitches from other breeders to incorporate into our breeding program. We also continue to co-own our outstanding young dogs with other breeders and watch them grow up in the hopes of being able to breed to them at a later date, if they are not affected.

We have also recently tried an experiment, that other breeders are claiming success with, to determine if young dogs are affected. Our young dog Can/Am Ch. Silhouette Surrender To Chriscendo had as a puppy a grey puppy coat that we thought might be suspect, so we shaved him down and put him on melatonin for a few months. Our experience with melatonin is that if a dog is affected the re-growth either does not happen at all or comes in as a cottony textured coat without guard hair. Within a month he began to grow his coat out, and within 6 months had grown a brand new, healthy double coat and won back to back Bests in Show his first two shows as an adult. Since then he won BW at the DeMoines Pomeranian Specialty where the judge commented on the correctness of his coat. What is more encouraging is that now as a two year old he has gone through a normal shed and continues to grow healthy orange hair. Unfortunately the usefulness of this experiment won't be known until the end of the life of the dog.

We were very pleased with the progress to date but until a genetic marker can be found we must consider all Poms as carriers until we can prove they are not. We have seen progress in our puppies in 2010. We have produced only one with a suspect coat and she will not be used for breeding. All of the dogs and bitches in our breeding program today are fully coated. We will not knowingly breed to an affected dog and we will eliminate any affected dogs from our program. We continue to evaluate our puppies show potential based on normal coat growth coming in at 4 months as one of the criterion.

We continue to participate in any medically based research and supply blood samples and pedigrees for testing. We extend an open invitation to any breeder, worldwide, who wishes to visit our kennel. 

Our continued research into Alopecia has lead us to discover that an intollerance to Gluten( Grain) is know to cause Alopecia. With this new knowledge we began feeding all the poms only grain free foods from weaning to adult. This was about 4 years ago and the results appear very promising. Since changeing to this diet we have not produced a single puppy with an abnormal coat. Usually there would be a percentage of abnormal coats even using fully coated dogs for breeding..

Our Statement regarding euthanizing juvenile BSD puppies.

Our litters are registered at about 3 weeks old which indicates the number of puppies in each litter. Each puppy is easy to account for and full records are made on their individul pages indicating their new homes at 3 mths. .Puppies that we run on after 3 mths are either kept, placed, or go to show/breeding homes depending on their potential. Each and every puppy is easily tracked. Ourbreeding records, if audited, would prove that no puppies are euthanized fo BSD. Our Veterinary records have been examined by staff and we have a signed letter from our Vet Clinic that not a single puppy has ever been euthanized for BSD. We also have signed lettersr from former employees who lived on the premises over the past 40 years which state that they have never seen or known of a puppy or adult euthanized for BSD. Any statements contradicting the above would be false.

Designer Genes
Genetic Management or Misery?
By: Catherine McMillan

In the early 1970s, Miniature Schnauzer breeders embarked on a
program unprecedented and unduplicated in any popular breed: to
eliminate the genetic defect that caused juvenile cataracts. Research
had established that juvenile cataracts (CJC) were transmitted as
autosomal recessive with complete penetrance and were present at
birth. Early diagnosis permitted the use of test-breeding, sanctioned
by the national breed clubs, in which certified affected dogs were
paired with mates whose status was unknown. A litter of normal eyed
puppies was known to generate a mathematical probability that the
tested dog was clear (the more normals, the better his or her odds),
while the diagnosis of a single affected puppy proved the dog a
carrier.
There is no argument that the program met its goals. A breed with an
estimated 40% carrier rate emerged from two decades of test breeding
with show lines cleared of the defect. It was a spectacularly
successful example of how a breeding community can come together to
eradicate a defect? and cause devastating damage to the gene pool.
Enter Stage Left
It has been written that, as a result of the process to eliminate
CJC, over 200 American Champions were retired from breeding.
Important kennels quietly closed up shop, taking distinct family
branches with them, and bitches were sent exclusively to test-bred
stud dogs. It was a lonely time for an untested male.
Around the same time as CJC was defeated, PRA made its entrance. In a
few short years, several leading sires were revealed to be carriers
and retired. There was no test-breeding program for this late onset
defect, so it became a lonely time for the stud dog or bitch with a
carrier ancestor. The gene pool contracted again.
Had this been the end of the troubles, there may have been time to
pause and reflect on what was happening in the big picture, but this
was not to be. A novel defect appeared on the scene ? a muscular
disorder called myotonia congenita. This problem found a solution in
short order as a DNA test was developed, allowing breeders to
identify carriers with a simple blood test. Those were retired, too.
My choice of the word "retired" has, of course, been deliberately
inappropriate here. In the world of dogs, "retired" is usually a
euphemism for "sterilized". As a device for preventing genetic
defects, it must rate as one of the most destructive practices ever
employed.
In a sensible dog world, quality carriers of genetic disease might be
pulled from widespread use, but they'd come out of "retirement" for
special occasions (i.e., for research breedings and/or the general
advancement and preservation of rarer family lines). However, the dog
fancy ? and, by extension, breed clubs ? have never been famous for
our ability to apply knowledge sensibly. There is a common caution
against throwing the baby out with the bathwater. In purebred dogs,
there is a tendency to gather up the siblings, cousins and parents
and throw them into the dustbin as well. We "improve" our breeds by
killing them off one family branch at a time.
When I first began breeding nearly 30 years ago, I accepted the
conventional wisdom that largely prevails to this day - that genetic
defects are the exception, that carriers should be removed from the
gene pool and that health is more important than beauty.
But, as John Maynard Keynes said: "When somebody persuades me that I
am wrong, I change my mind. What do you do?"
Managing the Unmanageable
A few years ago, some bright bulb at the Canadian Kennel Club
launched a grand scheme to create a Code of Ethics. One of the rules
proposed for this set of stone tablets was "Thou shalt not breed a
carrier". I recall writing to one of the Board members at the time to
congratulate the CKC for devising an edict that would result in the
immediate eradication of a number of breeds. For there are breeds
today in which every single member is not merely a carrier, all or
nearly all are affected with a genetic defect. The peculiar nature of
Dalmatian urine chemistry is the most famous example.
Even in breeds with more moderate disease rates, the policy would
have eventually resulted in genetic collapse and extinction. That's
because every normal living being is thought to carry in the range of
5 disease mutations in their DNA. In breeds with few founders and
extreme bottleneck events, that average may be much higher. As
molecular genetics digs into the DNA of our four footed friends, it
is revealing gene frequencies that are nothing short of staggering in
some breeds. In English Springer Spaniels, for example, a mutation
that elevates the risk of PRA has been identified and a DNA test
developed at the University of Missouri-Columbia. Of the dogs tested,
only 20% have been found to be clear of the gene while over 40%
tested as affected. Dobermans have similar carrier rates for the
bleeding disorder, vWD.
Time for a Change?
The purpose of this article is not to cover the ground of nuts and
bolts genetics. There's simply not enough space and I don't have the
right letters after my name. There are many good texts available that
cover the science, as well as a number of authoritative Internet
sources. It is recommended that you seek the most recent material you
can find as many of the popular canine genetics books of the past are
now obsolete.
What I hope to provoke is an examination of some of our traditionally
held beliefs. "Thou shalt not breed a carrier" served us well enough
when diagnostics were primitive, most carriers escaped detection, and
conditions now known to be inherited were dismissed as environmental
or simple bad luck. This is no longer the case.
Unfortunately, a little knowledge can be dangerous. The discovery of
extreme carrier rates in a breed has the potential to overwhelm
breeders who have always held that their primary goal was to produce
healthy dogs. It's depressing to think of how many aspiring breeders
accepted as an article of faith that quality foundation stock, good
intentions and careful testing would result in good health - only to
fail. They'd start over, fail again, become discouraged and move out
of the sport. Now we know why.
The bottom line is that much of what we thought was wrong. Now, for
the sake of our breeds, we need to change our minds. It is no longer
a question of "eliminating" gene defects from a breed. We can only
ask which ones, how quickly and should we even try? For this reason,
it is imperative that breed clubs take the lead and reform outdated
notions about "ethical" breeding practices and the advisability
of "retiring" animals before they can leave positive contributions to
the gene pool.
Diversity is Key
One of the most important factors in maintaining a healthy breed
population is preserving genetic diversity. Genetic diversity is
important for survival and adaptability within species, but dog
breeds are not species. They are purpose-bred populations that have
undergone selection for specific traits or behaviours. It is not
enough to simply survive; they have a job to do. Nonetheless, within
closed gene pools, genetic diversity is central to infectious disease
resistance and the availability of normal alleles when mutations
arise.
There is little disagreement on that point, but there can be great
disagreement on the best means to achieve it. One camp believes in
outcrossing, de-emphasis of "show ring" traits and performance
standards, and even selected infusions of other breeds. Another camp
holds that a healthy diversity of successful breeders who work to
preserve and develop distinct family lines is the best way to
preserve genetic choice. I happen to belong to the latter.
Before one begins, however, one must first define "successful". Or
rather, one must understand how success is defined in any breed. It
is not a matter of interpretation; it is a matter of record.
A few years after I began showing and breeding Miniature Schnauzers,
I realized that no historical archives existed for champion producers
in Canada, in the way they have always been catalogued in the US. So,
I began gathering the data from old CKC stud books and issues of Dogs
In Canada, starting with the first recorded champion in 1933.
Somewhere in the middle of the project, I had an epiphany. Everything
that I had been told to believe was wrong: Health is not more
important than beauty. Beauty is more important than health.
Next Issue: It isn't important that we all do the right thing, it is
only important that we don't all do the wrong thing. Forcing
everyone to do the same thing risks forcing everyone to do the wrong
thing.