AKC CHF Breeder's Symposium

AKC Canine Health Foundation Breeder’s Symposium

College of Veterinary Medicine, Western University of Health Sciences

Pomona, California

Saturday, April 4, 2009

I attended this symposium and was amazed at the amount of information presented! After UC Davis, Western University’s College of Veterinary Medicine is the only other veterinary medicine program in the state of California; they have only produced graduates for two years. Their program is the first new college of veterinary medicine in the United States in the past 20 years. As conference attendees, we also had the opportunity to tour the clinical learning center during lunch break.  

The room was filled with approximately 100 dog fanciers and breeders representing a wide cross-section of AKC recognized breeds. In an eight hour time period there were eight speakers scheduled. Each speaker could easily have spent the entire day trying to cover their subject matter and answering all our questions; but, alas, time was limited. Luckily some detailed information was included with the conference, including the book “ABC’s of Breeding” by keynote speaker Claudia Orlandi.

I’d like to try to summarize some of the important points from the seminar for the “Review” readers.

This lecture was my favorite!

“Current Concepts Regarding Canine Hip Dysplasia”

Peter Vogel, DVM, DACVS

Specialist in orthopedic surgery, critical care, microvascular surgery and is certified in stem cell regenerative medicine

From the syllabus:

“Breeders are an important source of information regarding heritable diseases such as canine hip dysplasia. However, much of what is common knowledge is often incorrect of incomplete. Find out the most recent information regarding the diagnosis and treatment of hip dysplasia and get practical recommendations that you can employ in your breeding programs. This talk will help you understand the limitation of OFA certification, the benefits of newer screening techniques, and give an overview of current treatment to help you educate your clients.”

OFA hip testing was initiated in 1966. After 40 years of OFA hip testing, the incidence of hip dysplasia in dogs has not decreased by even 1%. This is because hip dysplasia is a common defect; it is polygenic (multiple genes involved) and can also be exacerbated by environmental factors such as trauma and diet. Almost all lines of dogs have genes for hip dysplasia. This is probably due to the fact that the majority of dogs are descended from common original ancestors, who were themselves likely genetically predisposed to hip dysplasia. Greyhounds are rarely affected; sighthounds in general have a lower incidence than other races. Standard poodles are one of the very few breeds that are not commonly affected with hip dysplasia.

Hip dysplasia typically displays some symptoms by age 4-6 months. Symptoms can include pain/stiffness, pop or click of the joint, bunny hopping gait, and “lazy dog” syndrome. The dog will appear to the owner to be lazy, when in reality it does not wish to move because movement is painful. At age 12-15 months, signs and symptoms will disappear, only to reappear later in life when arthritic changes have set in. By then treatment methods are limited and expensive.

The OFA hip screening is the least predictive method for hip dysplasia. It does not rule out hip dysplasia. The OFA technique is outdated 1960’s methodology. The OFA screening xray is limited due to the positioning technique used; it is also subjective depending on those interpreting the film. A better method is the Dislocation Index (DI) which is also known as Penn Hip. Another newer and even more accurate method is the dorsolateral subluxation radiograph (or DLS) which is highly diagnostic for hip dysplasia. This technique positions the dog with weight on the knees and measures actual real laxity of the hip socket.

Fully 50% of dog who score OFA “excellent” hips will be found to be dysplastic using DI and/or DLS. 67% of those who score OFA “good” are actually dysplastic, and 100%  of dogs who score OFA “fair” are dysplastic.

DI technique has some breed-dependent factors (those factors were not discussed).

Another problem with OFA is waiting until the dog is two years old for their final evaluation. Hip dysplasia can and should be diagnosed by age 14-16 weeks and NO LATER THAN age 20 weeks, so that intervention can be done to prevent future painful arthritic changes.

If a puppy is diagnosed with hip dysplasia a simple procedure known as a Juvenile Pubic Symphysiodesis can be done. The growth plate of the pubis is cauterized to destroy the growing cells of this part of the pelvis. This results in a change in the angle of the pelvis and is 95% successful in preventing progression of the arthritis resulting from hip laxity. This should be done no later than age 5 months. It can be done at the same time as a spay.

A triple pelvic osteotomy can be done to reshape the pelvis; again this must be done before the age of one year and is very effectdive in preventing the progression of hip dysplasia.

OFA hip screening may not even be attempted in most cases until age two years (when it is too late to do any preventive orthopedic surgery), and it will miss most cases of hip dysplasia entirely.  Penn hip or DLS should be done on puppies no later than age 20 weeks for the most accurate diagnosis and early treatment of hip dysplasia.

Other ways to control the progression of hip dysplasia are weight control, proper exercise and diet. Medications such as NSAIDS and adequan have a proven track record. The benefits of glucosamine and chondroitin have not been clinically proven but those supplements can’t hurt. Stem cell therapy is in its infancy but may also prove beneficial.

In conclusion, the Dr. emphasized that if you are a dog breeder, sooner or later you WILL produce dogs with hip dysplasia. Don’t blame yourself! Even two dogs with perfect hips can produce dysplastic puppies. The genes for hip dysplasia are widespread through most every breed!

Common Household Toxins

John H Tegzes, MA, VMD, DABVT

An excellent overview of this topic. The ASPCA poison control number should be readily available in everyone’s home” 888-426-4435

Also, the National Poison Control hotline may be of use: 800-222-1222

Review of the many common toxins found in the home. Activated charcoal should be kept on hand and should be given to your dog if he ingests something toxic (use after consulting with poison control or your vet).

The lecturer told of a case they had where a dog ate snail bait and came in seizuring. They kept the dog alive on a ventilator and after 11 days of touch-and-go status in intensive care, he was sent home. The next day he was brought in again seizuring from eating snail bait. The owner didn’t pick up the bait because she figured the dog had “learned its lesson” and wouldn’t eat snail bait again!

The toxicity of raisins and grapes is very real and serious. Not all dogs are affected. The exact toxic substance within the grapes has not yet been discovered. Nor is it known if this may be a new genetic predisposition in dogs?

Walnuts are often contaminated with penitrem A, a fungal toxin.

Macadamia nuts have a neurologic sedating effect

A new dangerous toxic plant is broomfeldsia or the “yesterday, today and tomorrow” plant.

One of the attendees said her dog was poisoned by eating the inner stalk of the hibiscus flower. She had to search through 20 references on toxic plants before she found one that did list the hibiscus flower as toxic.

Canine Reproduction; Managing the Dog and Bitch to Optimize Success

Dana Bleifer DVM, DACT

Owner, Warner Pet Center, Rose City Veterinary Hospital, and owner/operator of CLONE West canine semen bank. Chesapeake Bay Retriever breeder.

Preparation of the dog and bitch is essential to breeding success. Avoid flaxseed and soy in food as it may in theory affect hormonal balance.

Thyroid test should be done on every bitch prior to breeding. TGAA (thyroglobulin autoantibodies) positive indicates autoimmune thyroiditis which is an inherited condition; in addition, thyroid autoantibodies can pass into the puppies from the mothers milk and attack their thyroid gland.

Brucellosis testing should be done periodically on all breeding stock, not just bitches.

Teeth should be clean as the bitch uses her teeth to sever the umbilical cord and can transmit bacteria to the puppy if her mouth is infected. Vaginal cultures are sometimes done but are not very useful because the vaginal tract is full of many different varieties of bacteria naturally. Sometimes you can find Klebsiella or mycoplasma with a vaginal culture; these would need treatment. However, if there is a suspected problem with infection it is better to bring the bitch in at the start of her season for a uterine culture. This is done with the aid of a fiberoptic scope. Routine use of antibiotics during the breeding cycle is not wise as you upset the natural balance of flora in the body. Antibiotics should be reserved for an infectious problem which has been demonstrated by a culture.   

A variety of insemination options were discussed, including the use of fresh, chilled or frozen semen. Ovulation timing using progesterone and LH levels was reviewed. Stud dog management should include a periodic semen evaluation, as well as regular prostate and testicular exams.

“The Canine Genome Decoded: An Introduction for Dog Breeders”

Christopher Irizarry, PhD

A presentation related to “bioinformatics”: the science of decoding the biological information contained within genes and genomes. The canine genome shares many similarities with other mammalian species, and differs from them just by a few small percentage points.

Dr. Irizarry explained how some genetic research is conducted. His team worked with mice and “knocked out” or removed one certain gene from the genome. The chromosome was then replaced into the breeding animal and offspring were tested to see if they were missing the gene. Then if they had two animals who both were missing the particular gene being studied, they bred those together to try to get offspring that were “doubled up” for the missing gene, then they would observe what effect this had. The found a gene that limited growth of muscle tissue (“myostatin”), which, when “knocked out” of the genome and “doubled up” offspring were completely missing this gene, the animals were extremely overmuscled. There were examples pictured of this effect in both mice and cattle.

“On Breed Identification: Visual and DNA”

Victoria Voith, DVM, PhD, DACVB

An interactive session comprised of a breed identification quiz. Photos of shelter dogs were taken, shelter workers were surveyed for each dog. They were asked  if the dog was purebred or a mixed breed, and if mixed, what were the primary and secondary breeds. The dogs’ actual breed composition was identified by DNA analysis and compared with the answers given by the shelter workers.

We seminar participants also took this breed identification survey. Results seemed to indicate that identification of breed makeup based on appearance is not reliably accurate.

“ABC’s of Dog Breeding”

Claudia Waller Orlandi, PhD

This was the keynote speaker, and all participants received a copy of her book, which is a wonderful explanation of dog breeding presented in a fun and easy to understand format.

Genetics, selection, breeding systems, pedigree analysis, canine anatomy, genetic defects and kennel blindness were all discussed, using an interesting slideshow. The book we received is a wealth of information! You can buy it from the website:

http://www.abcsofdogbreeding.com/

Some key points: The pedigree is not more important to consider than the dog itself. Also, linebreeding beyond the fourth generation will have little impact on a litter. No one part of the anatomy of a dog is more important than the whole dog.

In the seminar, discussion of inbreeding/linebreeding did briefly touch on inbreeding depression, and the hazards of doubling up on harmful recessive genes.

Popular sire syndrome is not mentioned.

The harmful effects of homozygosity on the immune system were never mentioned.

In fact, the speaker stated that we would all like to have dogs that are homozygous for all “good” genes. The evidence is available that genetic homozygosity is not beneficial except for being useful to produce some predictability in breeding results.

Inbreeding has been necessary to form some breeds but it has had the side effect of setting in defects into almost every breed. Further culling in attempt to remove those defects results in lack of genetic diversity which is essential for health.

Narrow breed standards and judging for the extreme “stand out” specimens who are extreme in type promotes unhealthy extreme animals.

Yes, we want to produce predictable type and soundness; but our dogs also need some genetic variability. Heterozygosity in general produces healthier animals, with improved vigor and stronger immune systems. This will promote vigor, longevity and strong immune systems for our breeds to remain viable into the future.

“Grooming from the Inside”

Deborah A. Greco, DVM, PhD

The speaker is a senior research scientist with Nestle Purina Petcare. Good quality skin and hair coat can be maintained through a well-balanced diet. Her contention is that commercial pet foods are the easiest choice when available for maintaining skin and coat condition in healthy animals. She further believes that caution and care should be used when prescribing supplements or homemade diets to ensure proper nutrient balance. “Food is the least expensive and most important grooming tool available to the modern day breeder.”

There was no mention made of melamine toxicity, aflatoxicosis, or the many problems associated with the overprocessed ingredients used in most all commercial pet foods.

Erika Werne gave a comprehensive overview of AKC’s CHIC program.

I’d like to thank AKC for this very interesting and valuable symposium; I hope that another will be presented in our area in the near future.

Chromosomes-Pull Up Yer Genes!

CHROMOSOMES-Get your Genes On!

Why is Spot larger than Rover? Why does Trixie have a golden coat while Muffie’s is black? And why are Muffie’s ears floppy while Rover’s stand upright?

Specific characteristics of living organisms are determined by their “GENES”. Genes are “coding” segments made up of a substance called DNA. The DNA in your genes is arranged in specific patterns. Different genes are strung together in long rows to form a rope-like chain called a “chromosome”. Each chromosome contains thousands of genes.

Chromosomes are instruction panels; they provide the blueprint to make an organism what it is. Chromosomes carry all of the information necessary to help living things grow, survive and reproduce. Chromosomes are located inside the cells of the body in a central control area called a “nucleus”. These chromosomes determine not only what you look like, but also how your body functions and, to a large extent, how you act, think and feel.

The DNA that makes up genes and chromosomes is like a computer code of instructions. Chromosomes s build a copy of themselves and send those instructions to other parts of the cell, the ribosomes, and the ribosomes in turn manufacture proteins according to instructions provided. These proteins might be enzymes for body metabolism, or proteins for building body tissues.

During normal cell division for growth or cell replacement and repair, chromosomes double and then split apart to form two cells from one. Now both of these cells will end up with identical chromosomes within their nuclei. However, there is a special type of cell division that happens to produce the reproductive or “germinal” cells. Instead of doubling, the germinal cells are produced by by splitting up the original chromosomes. These reproductive germinal cells, the sperm and the eggs (ova), therefore will contain only HALF the number of chromosomes as do the other cells of the body. When a sperm cell combines with an ovum, VOILA! there is then a complete set of genes with a full set of instructions to create a new living being. This new creature will have half his genes originating from his father’s sperm, and the other half will have been contributed by his mother’s ovum.

This process involves something known as “random fertilization”. What does that mean?

The chromosome combination contributed by a sire to his offspring is random, and can vary considerably. Half his chromosomes will end up in that sperm cell…but how many different possible combinations of chromosomes can there be in any one sperm cell?

Let’s check it out. Humans have 46 chromosomes, arranged in 23 pairs, that divide and split up to form germinal cells, and they assort independently. To form a germinal cell, there are 2^23, or 8 million, possible different assortments of chromosomes that could be produced for each individual cell!! The ovum also has 8 million possible different chromosome combinations. 8 million X 8 million = 64 trillion possible unique combinations of chromosomes for every human offspring created from any given mating! See how unique you are! Even your siblings may have quite a different genetic makeup than you do!

A human cell has 46 chromosomes, arranged in 23 pairs. A dog cell, however, has 78 chromosomes, arranged in 39 pairs. Each sire can produce roughly 550 BILLION different assortments of chromosomes in their sperm cells. Multiply that by the 550 billion possible combinations of chromosomes in the dam’s ova, and there are 300,000,000,000,000,000,000,000 possible DIFFERENT combinations of chromosomes that can be produced for any individual dog created from any specific mating.

WOW! that’s a lot of zeros. How do you read such a number? It is 30 billion trillion. This is roughly the same number as the estimate of stars in the visible universe. Each dog from any certain mating is as unique in his genetic makeup as a star! That's a very nice comparison, I think.

But wait! There is another factor that can further increase genetic variety in offspring. This is the phenomenon known as “genetic crossover”. Crossover commonly happens during cell division to produce sperm and ova. What does “crossover” mean? Let’s see….remember we said that each chromosome has a partner chromosome with similar genes on it. During cell division, part of one chromosome may break off and swap material with its partner. This means that sometimes the chromosome that you inherit is totally different from the original one your parent has. The crossover process “shuffles the deck” so to speak, to produce even more variety in offspring. It would be impossible to estimate how much more variety this effect produces! But we would need millions more universes filled with billions more stars to get close to the number of unique combinations of chromosomes possible with any specific mating.

This vastly inconceivable number implies a rich potential to produce dogs who have a very unique and highly individualized genetic makeup. This inherent variety in the dog genome is how man has been able to create so many different breeds with characteristics as different as those noted between a Chihuahua and an Irish Wolfhound. Compare the variety in dogs to that of humans, who all look remarkably similar….even people of different races. We have fewer chromosomes to reassort and recombine, and less chance of isolating and promoting different specific traits.

Now do you still think that one or two litters is enough to judge what your dog can produce? Although, I am sure there are animal rights “overpopulation” handwringers out there who believe that every intact dog will produce billions of puppies in just seven years. Hmmm, I only wish I could get more than three or four at a time to select from!

And just think, each and every chromosome contains thousands of individual genes! In the next issue, we’ll talk about how those genes combine and recombine to work their magic!

Pigment and Health

Pigment and Health Merle and White Spotting Genes This article was originally written in 2005, just prior to the identification of the merle gene and the subsequent development of the DNA test for merle, and the 2007 discovery of the MITF as the gene responsible for "S" white spotting. It has been updated to reflect these discoveries. The Relationship of Pigment to Health by Geneva Coats, R.N. Rare and exotic colors...one of the most attractive and exciting features of our Pomeranians. Variety is the spice of life! Different styles appeal to different breeders. However, there are some important pigment-related health issues to consider. BREED STANDARDS Since the inception of purebred dog registries, standards have been established for all breeds. The standard serves to protect a breed from fashion whims. It strives to maintain a breed's traditional "look" and purpose. The standard establishes desirable conformation goals, temperament characteristics, and suitability for the original purpose of the breed. The standard provides a goal for breeding practices. This is why standards are written in the first place, to act as guides for breeders and judges. You don't need to understand all the details and theories of genetics, but you do need to abide by the standard when breeding and judging. Our Pomeranian standard was changed in 1997 to allow all colors, patterns, and variations thereof. This may serve to promote some breeding practices which might ultimately be detrimental to the health of the breed. We need to examine this issue carefully. The direction we take in breeding is the path to our future. The desire for health and concern for future generations must always take precedence over the desire for aesthetics. Why is a color or pattern so important to the stewards of a breed? Breeders have always been keen scientific observers, even before genetics became an established field. They have worked tirelessly toward a goal of producing healthy dogs. Dog with health issues are in limited demand as companions, and often unsuitable for work. Some breed standards disallow excessive white, dilute colors or merle. Many breed standards specify that parti-color dogs have a certain proportion of color to white, or that they must have color extending over both eyes and ears. Most all standards call for full, dark pigmentation of nose, lips, eye rims and pads. Albinism is generally disallowed. These guidelines were not established for aesthetics' sake, but because certain colors, patterns, and lack of pigmentation were known to be associated with an increase in certain specific health problems. There is much documentation and information related to the merle and white spotting patterns, and they will be the focus of this article. COAT COLOR DEVELOPMENT The process of coloration and color patterns in dogs starts with embryonic development. The cells which become melanocytes (pigment producing cells) are derived entirely from the neural crest of the embryo. Pigment cells develop from the same cells that give rise to the nervous system. Defects in certain color genes can be associated with defects in the nervous system, as evidenced by vision and hearing problems. Color provides a logical genetic indicator, and explains why it is likely that certain patterned dogs, such as extreme piebalds (>90% white) and merles may be at risk for specific health problems. In studies to date, the coat patterns resulting from genes producing white are significantly associated with deafness. In addition, suppression by "white genes" of pigmentation in the iris of the eye is also associated with deafness. On the other hand, the presence of pigmented, colored patches in the coat is associated with reduced risk of deafness. WHAT IS MERLE? Merle is regarded as a coat pattern, not a color. The merle gene works like other dilution genes, in that it lightens whatever color is already there. Whatever the basic color of the dog-unless he is all white-the merle gene will cause dilution and splotching imposed on the base coat color. The appearance is a speckling or marbling, like when bleach is splashed on your clothes. The pigment cells are affected individually in the fetus. Some are disabled completely, leaving white areas. Some cells allow partial expression of pigment, leaving merled or dappled areas. Some cells are unaffected, leaving the coat color normal or non-merled. The amount of dappling or merling can vary. The dog can have perhaps just a small dappled spot somewhere, or perhaps just a light eye with a nondappled, normal coat. Or, it might display dappling throughout the coat. The effect is most noticeable on a black coat; where the black is diluted to grey, the color is called "blue merle". Merle appears at first glance to be dominant, because if a dog carries one gene for the merle factor, he will be affected by it. However, merle is different, because it is incompletely dominant. A single merle gene, inherited from one parent, produces what is known as a "heterozygous" or "single" merle. This single copy of the gene will usually cause the affected dog to display merling somewhere in the coat. This can range from light dappling to extensive dappling. Sometimes the effect on the coat is not evident, and there is no way to tell at maturity that the dog carries the merle gene. Sometimes, blue flecks in the eyes are the the only sign that a dog carries the merle gene. If two heterozygous merles are bred together, statistically 25% of the offspring will inherit two merle factor genes, one from each parent. When this happens, we produce what is known as a "Double (homozygous) merle". The effect of the gene is then doubly intense. There is so much color dilution that the dog is usually predominantly white, and almost always has impaired hearing or vision-or both. In Great Danes, merle interacts with another gene called harlequin, which bleaches the gray areas of the coat to white. In the pure homozygous form, harlequin is lethal. In Danes and Aussies, the tweed pattern is a variation on merle which adds a third, intermediate shade to the coat. Many double merle dogs are so defective that they do not survive to birth. (estimates are as high as 50% mortality in utero). Those that survive are the ones with "just minor" defects...minor enough to handicap rather than kill. A gene that destroys half of those carrying it in a double dose in utero cannot be dismissed or ignored. In French, the word "merle" means "blackbird", and "le merle blanc" ("The white blackbird") is an expression, meaning something that is impossible or something that cannot exist. This is an admirable goal for the white merle dog! HOW MERLE WORKS Merle is a gene that is inherently unstable. It is a "transposon", or transposable element; a mobile parasite segment of DNA in the chromosome. Transposons usually originate from viruses. A virus is a particle containing DNA which inserts itself into the host cell, thereby infecting it. If the virus does not kill the host cell, it can leave behind a piece of its genetic material in the DNA of the host cell. When this happens in the sex or germinal cells, the particle can become a part of the genetic makeup of some of the offspring. This is a way that mutation occurs. Transposons have also been called "junk DNA or "selfish DNA", as they rarely provide any benefit to the host cell. Transposons are also often referred to as "jumping genes." The transposon can move to different positions in the cell in a "cut and paste" process. In so doing, it may cause mutations, or alter the amount of DNA in the genome. The merle transposon segment may lose some of its DNA particles during cellular replication during early embryonic development. Coat color in that area will then be less affected by the gene, or even unaffected, and the underlying true coat color will be expressed. This explains why there are some areas of the coat which are NOT dappled, and other areas which ARE. The decorative variegated Indian corn is produced by transposon elements in the corn gene. Many viruses, such as those responsible for AIDS and feline leukemia, function as transposons. In humans, hereditary diseases such as hemophilia A and B, predisposition to colon polyps and cancer, and Duchenne muscular dystrophy, are all related to inherited mutations produced through the transposon process. Genetic engineers sometimes use transposons to try to intentionally introduce certain genes into an organism. There are also documented cases of homozygous merles producing non-merle offspring ("germinal reversion"). This is further evidence of the instability of the gene. Not only can you sometimes get non-merle pups (which should not happen according to the rules of Mendelian genetics), but worse things can happen. The "cleft palate syndrome" is a rare and isolated Aussie defect that has been the subject of numerous scientific journal articles and symposia presentations. It is a sex-linked (on the X chromosome) defect, in which females have minor abnormalities, like extra toes, while males die of massive skeletal abnormalities and a cleft palate. This disease started with a homozygous merle bitch that was kept for coat color research. PIGMENT PLAYS A ROLE IN HEALTH Many breeds have the white spotting and merle factors in their gene pools. These genes are not colors per se, but do affect the expression of coat color. In breeds which have traditionally included the merle color pattern, the predominantly white (double-factored) merle has been disallowed in the show ring, as well as selected against in the whelping box. And with very good reason. The gene which produces the merle pattern is associated with some very serious health defects. Both the white spotting gene and the merle gene are known to sometimes affect hearing. The merle gene, however, is unique in that it interacts in an as-yet undetermined manner with genes for eye features. MERLE AND EYESIGHT There is a complex of eye defects associated with the merle gene. These defects can be superficial in nature, such as a difference in color between the iris of one eye and the other. The example of this is a dog with one brown eye and one blue eye. (Note that this trait is not necessarily indicative of possession of the merle gene, because it can also be found in dogs with extreme white spotting). In addition to superficial indicators there are also major effects, such as absence of the reflective substance which lines the back of the eye, resulting in reduced ability to see in low light. There can be lack of retinal pigment, which directly reduces vision. Small or absent eyeballs, irregular or starburst pupils, and clefts in the iris can occur, as well as persistent pupillary membrane, strabismus (cross-eyed), lens luxation , and juvenile cataracts. THE MERLE LINK TO MICROPHTHALMIA The term "microphthalmia" means a smaller than normal, tiny eyeball due to a defect in early development. Microphthalmia is a defect very commonly associated with merle; particularly homozygous "double" merle, it even rarely occurs in heterozygous or "single" merles. Complete absence of the eyeball in the eye socket sometimes occurs. This is known as anophthalmia. MITF, or "Microphthalmia Transcription Factor", was discovered in 2007 to be the location of the gene that affects pigmentation, causing white spotting (otherwise known as the particolor or piebald pattern). The merle gene is believed to affect eye development through some sort of interaction with MITF. Now, why would microphthalmia occur in association with merle and not just with white coat color in particolor dogs? I've asked several canine geneticists, but have received no answer! This relationship is still a mystery. The exact mechanism by which merle interacts with the white spotting gene and produces the defect of microphthalmia is still waiting to be discovered! MERLE AND HEARING Hearing impairment can occur in merles due to a lack of melanin or pigment in the inner ear. Not all merles will develop problems with hearing, it all depends on whether or not the inner ear is pigmented. If the inner ear isn't pigmented, the nerve cells responsible for hearing can't develop as they should. Then, the nerve endings atrophy and die off in the first few weeks of the puppy's life, resulting in partial or total deafness. The deafness is neither dominant nor recessive, but is linked to the merle gene which disrupts pigmentation and secondarily produces deaf dogs. White outer ear color is often associated with lack of inner ear pigment and deafness. However, sometimes deafness occurs even with patches of color on the ears. Mild to moderate hearing impairment may never be noticed, and is rarely tested for. ONE COPY OF THE GENE HARMLESS? The popular belief is that heterozygous merles are completely normal, and that only homozygous merles have health defects. Heterozygous merles can have expression of lesser defects of the eye such as clefts in the iris, and a thinning of the retina (similar to what is found with Collie eye anomaly). There are also rare cases of microphthalmia in "single" merles. Deafness can also sometimes occur, if the merle gene prevents pigment deposition in the nerve cells of the inner ear during embryonic development. Heterozygous "single" merles often have reduced eye pigment which produces the characteristic blue eyes. Interestingly, the amount of white even in homozygous merles does not correlate to severity of eye defects. In a study of the embryonic origin of merle eye defects, Dr. Cynthia Cook, of the University of California, San Francisco, observed that the severity of eye defect and amount of pigment were not related. This is in contrast to hearing impairment in merles; the likelihood of deafness increases with increasing amounts of white in the hair coat. The Hannover Veterinary School in Germany conducted studies on Dapple (merle) Dachshunds. Their studies demonstrated eye problems, sperm imperfections, and hearing impairment. These problems were found in homozygous merles, and also heterozygous merles. Hearing faults, ranging from slight hardness of hearing to complete deafness, occurred in 54.6% of homozygous merles and 36.8% of heterozygous merles. As a result of these studies, in 1986 it was suggested that FCI restrict the breeding of merles on welfare grounds. These studies, however, are now generally considered outdated. Future testing of vision and hearing in merle dogs will hopefully paint a clearer picture for us. GENETIC LINKAGE CAN CAUSE SPREAD OF DEFECTS Genes on the same chromosome are usually inherited together. However, during cellular division and replication, sometimes chromosomes will randomly break and recombine. Genes that were formerly associated with each other can then become separated and inherited independently. This process is known as genetic linkage. We have already mentioned the Aussie cleft palate syndrome which originated with a merle bitch. Iris coloboma, or missing part of the iris, is being reported in non-merle Aussies. Coloboma appears as a notch at the edge of the pupil, giving the pupil an irregular shape. This sight-altering defect is believed to have been brought into the breed through linkage with the merle factor. This trait is now inherited independently from merle. It is likely more than coincidence that breeds in which merle is most common are also breeds which are heavily plagued with a variety of eye defects. Yearly CERF testing by a veterinary ophthalmologist can help screen out heritable abnormalities. Further studies in merle dogs are needed to observe the frequency and exact methods by which eye defects are produced. It is theorized that some mutations are produced by damage done to portions of the chromosome located near to the erratic merle transposon. BREEDING RECOMMENDATIONS FOR MERLE Sometimes a dog is genetically carrying the merle factor gene, but there are no outward signs (cryptic or phantom merle). This dog could easily be inadvertently bred to another merle and result in the production of homozygous double merles, so for this reaon it is usually recommended to avoid breeding merle to brindles or any purely phaeomelanin (orange-red-gold-yellow) coat colors. It is almost universally recommended to NEVER breed two merles together, to avoid producing defective double merles. But, unfortunately, some breeders will intentionally breed merle to merle, hoping to produce a higher percentage of merle offspring. This is sadly a misinformed idea. Others may breed merle to merle in an attempt to produce a double merle sire to use for future breeding. Such a double merle dog (even if vision or hearing impaired) will produce 100% merle offspring. There is a demand for the unusual merle color. Although this method of breeding may be considered unethical, it does happen in many breeds, by uneducated or uncaring breeders. A merle dog should be bred to a dark colored mate, preferably black or black and tan. A dominant black dog will only produce black offspring half the time, unless he carries two copies of the dominant gene for black. Couple a black with a merle parent, who will produce merle offspring 50% of the time, and the odds just dropped to 25% for producing a blue merle from a black to merle mating...the same odds of producing a sable merle or hidden merle from such a breeding. Black and tanpoint pattern is recessive and would breed true. If one parent is also merle, you have a 50/50 chance for producing blue merle offspring, and 50/50 tanpoint who are not merle. Recessive black would also breed true, just as black and tan does, but recessive black seems to occur only very rarely in our breed. Also, In our breed, there is a widely carried recessive gene "e" which suppresses all black pigment in the coat. This gene can double up in the offspring to hide the visual appearance of merle. Here is part of a statement by canine geneticist Sheila Schmutz, written for the Pomeranian standard revision committee in April 2006: "Yet another gene in the "blue" family that can cause health issues is merle. Merle can not be seen in dogs with an e/e genotype. This e/e genotype occurs commonly in Pomeranians since orange, red and white probably account for the majority of Poms. The problem is that M/M (homozygous merle) dogs are always deaf based on our studies. We recently genotyped 24 mostly white Australian Shepherds and all tested M/M (based on the Clark et al. 2006 PNAS published test) and all were deaf. A proportion of these dogs were also blind in one or both eyes since microphthalmia is another common side effect in M/M dogs. Although in many breeds it is possible to educate breeders to never breed two merle dogs together this advice is not possible to follow in Pomeranians since e/e dogs would not show the merle pattern. It would therefore be necessary instead to advise all persons who breed a merle dog to use only a black or sable mate or to have DNA testing done on their red, orange or white mate prior to breeding to be sure it did not carry merle." Further complicating the picture is the case of breeding a merle to any dog with excessive white in the coat. Breeding merle to parti-color dogs with more than 50% white coat is advised against; especially if the merle parent also carries genes for particolor or "white spotting". It would be difficult to determine if the resulting puppies were merle or extreme piebald white-or both-without DNA testing! In either case, hearing can be affected. DNA TEST FOR MERLE We now have a DNA test for merle! This is a wonderful tool for breeders who choose to avail themselves of the technology. A cheek swab from the dog is sent to the lab, and they can tell you if your dog is merle or not. This test can also tell you if your dog carries one copy or two copies of the gene. Unfortunately, the US company offering this test closed its doors in March 2009. However, another company (Idexx) is poised to take over this service. Here is the link to the Idexx website: http://www.idexx.ca/diseasesinseason_profile.cfm Unfortunately, the merle test costs close to $100, so some breeders will not o use the test, even when available. These breeders continue to try to guess the merle status of their dogs solely by appearance, noting the amount of dappling and/or white coat color. AKC registration for Pomeranians now allows for designation of color as merle. However, this will remain an inaccurate system unless breeders DNA test all questionable offspring from their merle parents. Currently, merle is uncommon in the Pomeranian breed. However, as the pattern becomes more popular and widespread, it will more likely show up when least expected in a breeding program. WHITE SPOTTING AND HEARING Another pattern gene strongly associated with deafness in dogs is the "S" series-commonly known as white spotting, Irish spotting, or piebalding. Breed examples are the Bull Terrier, Samoyed, Greyhound, Great Pyrenees, Sealyham Terrier, Beagle, Bulldog, Dalmation, English Setter, Papillon and Fox Terrier. The recessive "S" gene covers the coat color with white, and when weakly expressed allows patches of color. This process is believed to be related to the path of migration taken by the pigment cells in the embryo. During fetal development, the melanocytes (cells that produce pigment) are concentrated in the neural crest. The neural crest is the area which eventually becomes the brain and spinal cord. From the neural crest, the pigment cells migrate to the peripheral areas of the body, such as the head, legs and tail. However, sometimes the melanocytes don't travel completely over the body. Any areas where the pigment cells fail to migrate will remain white. This is why sometimes dogs will have a white spot on the end of the tail, the tips of the toes, or on the chest. If pigment-producing melanocytes fail to reach the inner ear, deafness will result. White color on the head is often, but not always, associated with lack of inner ear pigment. Patched-colored dogs with dark eyes have been selected for in many breeds. These dogs have reduced incidence of hearing impairment when compared to dogs which are almost totally white. Not all breeds with the "S" -extreme piebald pattern have been reported to be affected with deafness, and there is also inherited deafness in several breeds which is totally unrelated to coat color. HEARING TEST The only way to know for sure if your dog is hearing impaired is through a Brainstem Auditory Evoked Response Test, or BAER test. This testing is only available at select facilities and can be expensive. It need only be performed once in a dog's lifetime (preferably at a young age) to rule out hereditary hearing impairment. A complete list of BAER testing facilities can befound on Dr. George Strain's website: www.lsu.edu/deafness/deaf.htm. Selective breeding for hearing dogs, as evidenced by normal BAER testing, can reduce the incidence of deafness in dogs, including those with high risk factors. OTHER PROBLEMS Other health concerns associated with lack of pigmentation are skin allergies, skin cancer and sunburn, demodicosis (immune-mediated hair follicle mange), follicular dysplasia (coat which is dull and breaks), reduced fertility and sterility, and photo-induced epilepsy. CONCERNS RELATED TO THE PRODUCTION OF HANDICAPPED DOGS Some animal welfare specialists endorse humane euthanasia for all dogs deaf in both ears (bilaterally deaf). Hearing can not be accurately assessed before 5 weeks of age. At this age, euthanasia can be an agonizing decision for any caring, ethical breeder. Deaf or blind dogs require special placement arrangements. A breeder is morally and ethically responsible for care and placement of handicapped dogs. We may see in the future an increase in handicapped Pomeranians turned over to rescue or to shelters. As there are always so many healthy dogs in shelters and rescue who cannot find homes, the odds of finding homes for handicapped dogs are even greater. Support for rescue from our parent and regional clubs will likely need to increase. WHERE DO WE GO FROM HERE? Many people have voiced concern that the merle pattern has only recently been introduced to our breed, through crossbreeding with merle dogs of other breeds. However, all breeds have been created through such methods at some point in their history. The concern is not so much HOW the pattern appeared in our breed, but rather WHERE it will take us in the future. APC is the parent club for the Pomeranian, and as such, should serve the breed with the commitment and resonsibility that the word "parent" implies. It is a responsibility of a parent club to discourage breeding that is known to increase the probability of dogs with health problems. This can be attempted through education of breeders and the public. Such education can be provided on the club website or through the person designated as health and genetic liaison. Education should include factors to consider in selecting a canine companion, as well as methods of developing a breeding program with an emphasis on producing healthy offspring. Public awareness of health issues may eventually create an increased demand for dogs bred as much for good health as for physical beauty. Many breed clubs promote responsible breeding through the breed standard Itself. (For instance, our Pomeranian standard stipulates that eyes must be dark). Guidelines can also be provided through a breed club's code of ethics. The guidelines might contain recommendations such as: 1. Yearly CERF testing for all breeding stock, particularly merles. (Clinics should be made available at national and regional specialties). 2. BAER testing should be performed once in a dog's lifetime prior to breeding. This is especially important in merle and extreme piebald patterns. 3. All dogs from merle litters be sold only to knowledgeable breeders or transferred to new owners after being spayed or neutered. This will help prevent uneducated breeding and the production of handicapped dogs. 4.Vision and hearing health should be guaranteed in all puppy contracts, Dogs so affected should be readily taken back by their breeder at any point in their lifetime. 5. Any puppies from a litter with a merle parent who do not appear to be merle should be DNA tested to determine merle status, (unless of course they are going to be sterilized, in which case DNA merle testing would not be necessary). As breeders, we need to avoid the ostrich syndrome. Let's not stick our heads in the sand and hope problems will go away....they might get worse if we do! STUDY!! We should learn all we can about genetics and heredity-of all breeds, not just our own. The other guy's problem today may well be ours tomorrow. SUMMARY Our breed already has some health concerns. It would seem unwise to encourage an increase in defects purely for the sake of novel color patterns. Through education and personal responsibilty, risky breeding practices can be minimized. We should strive to produce puppies blessed with the gifts of normal vision and hearing. If this article serves to prevent the birth of just one handicapped dog through heightened breeder awareness, it will have been worthwhile. PIGMENT-RELATED DISORDERS IN HUMANS One in 17,000 persons in the USA has some type of albinism, as indicated by little or no pigment in their eyes, skin, or hair. People with albinism always have problems with vision. This results from abnormal development of the retina and abnormal patterns of nerve connections between the eye and brain. It is the presence of these eye problems which defines the diagnosis of albinism. Albinism may be limited to the eyes or involve hair and skin to varying degrees. Waardenburg syndrome is an inherited disorder in humans characterized by varying degrees of hearing loss and changes in skin and hair pigmentation. This syndrome was named for the Dutch ophthalmologist who noticed that people with pigmentation abnormalities of the hair, eyes and skin, often had hearing impairment.Those with Waaardenburg syndrome may have two differently colored eyes, one brown and one blue. Sometimes, one eye has two different colors. Others may have unusually brilliant blue eyes. People with Waardenburg syndrome also have distinctive hair coloring, such as a patch of white hair near the forehead, or they might have white patches of skin. Waardenburg's is associated with other birth defects such as spinal or intestinal disorders or cleft palate. After doing this research, I finally realized why I reach for sunglasses each and every time I go outdoors on a sunny day! I have blue eyes, and cannot tolerate the bright light. My eyes lack sufficient light-blocking pigment! Sincere thanks to TAMU's Leigh Anne Clark, PhD for answering my many questions. You are wonderful! http://www.cvm.tamu.edu/cgr/merle.htm Thanks to Sheila Schmutz, PhD for her expert advise on canine color genetics: http://homepage.usask.ca/~schmutz/dogcolors.html Thanks to JP Yousha for her color genetics expertise! Your input was invaluable. www.chromadane.com REFERENCES Anderson, Cheryl, "Theories of Color and Pattern Dominance in Shelties" Bowling, Sue, "Canine Color Genetics", "Elementary Merle Genetics for Newcomers", "Basic Genetics, the Relationship of Genes to Traits" Cattanach, Bruce M., "The Dalmation Dilemma: White Coat Color and Deafness" Chopson, Jane, "Inheritance of Great Dane Coat Color" Sept 1992. Dowd, Scot E, PhD, "Health and the Merle Pattern", American Dog Breeders Association Little, Clarence C,. The Inheritance of Coat Color in Dogs, 1957. Sharp, C. A., "Can You See? Inherited Eye Diseases in Aussies", "Genetic Nightmares", "The Trouble with Merle", "White Fright". Strain, George M. "Deafness Prevalence and Pigmentation and Gender Associations in Dog Breeds at Risk". May 15, 2003. Strain, George M., "Hereditary deafness in Dogs and Cats: Causes, Prevalence, and Current Research." Oct 2, 2003. "The Merle", United States Border Collie Club Newsletter, Winter 1995. Willis, Malcolm B. Genetics of the Dog, 1989 Willis, Malcolm B., "Merle Chihuahuas-Time to Call a Halt" Our Dogs, Feb. 17, 2005. Yousha, J. P., "Whites; is it Worth the Risks?" Yousha, J. P., "The Harlequin Family of Dogs: Harls, Merles, Blacks, Whites and More." INTERNET RESOURCES http://www.ashgi.org/color/eyedefects.htm www.tanyastoys.com/drwillis.htm www.dachshund.org/article_double_dapple.html www.offa.org/deafgeninfo.html www.jabed.com/rcas.htm www.lsu.edu/deafness/deaf.htm www.deafdogs.org www.blinddogs.com www.eyevet.info www.mascaonline.org/Health.htm www.ashgi.org www.whiteaussies.com www.chromadane.com www.bowlingsite.mcf.com/genetics/genetics.html www.albinism.org/publications/what_is_albinism.html www.albinism.org/publications/HPS.html www.nidcd.nih.gov/health/hearing/waard.asp www.answers.com/topic/transposon-1 http://waynesword.palomar.edu/transpos.htm

Copyright 2005. Revised 2009.This article may not be reproduced or distributed in any form without express written consent of the author.

The Emperor's New Study

The Emperor's New Clothes Study

Hear ye, hear ye!

New study proves (beyond the shadow of a doubt) that:

Purebred Dogs are Just as Healthy as Mixed Breed Dogs!

Carry on with the mission! Inbreed; linebreed! It's not a problem! Breed to the most popular sire, so you too can have a chance to prevail supreme in the jousting tournament of dog superiority!

We are advocates for health testing, but we don't worry about the risks of narrowed gene pools! That would simpy be too upsetting to the apple cart!

Today I read an article about how AKC wants to "clarify misconceptions about purebred dogs." (a) For one of those "misconceptions" the author cites a recent study comparing the health of purebred vs. mixed breed dogs. The author claims that this study affirms that purebred dogs are just as healthy as mixed breed dogs. 

In actuality, the UC Davis study shows that for heritable health problems common to most dogs, mixed breeds are just as susceptible as purebred dogs, while for many more breed-specific health problems, purebred dogs are more susceptible than mixed breed dogs. This "news" should not come as a surprise to anyone familiar with the science of inheritance and genetics.

However, this same study is continually touted in social media sites and in news releases from the AKC, as some sort of ultimate proof of the undisputed superior health of purebred dogs. Similar to other "Big Lies", there's a belief that if something is shouted loudly enough, everyone will believe it!

Well, not quite EVERYONE. In fact, the American Veterinary Medical Association examined that same study and came to the exact OPPOSITE conclusion:

"STUDY SHOWS MUTTS GENETICALLY HEALTHIER"

"The researchers concluded that modern purebred dogs or members of similar lineages appeared to be more susceptible to certain inherited disorders. Disorders occurring equally among purebreds and mixed-breeds suggested that the disorders represented more ancient mutations and were more widely disseminated throughout the canine population." (1)


And the conclusion itself on the published study on Pub Med states:

Recently derived breeds or those from similar lineages appeared to be more susceptible to certain disorders that affect all closely related purebred dogs, whereas disorders with equal prevalence in the 2 populations suggested that those disorders represented more ancient mutations that are widely spread through the dog population. Results provided insight on how breeding practices may reduce prevalence of a disorder. (2)

But, unfortunately, the results did NOT help the willfully ignorant to understand "how breeding practices may reduce the prevalence of a disorder."

THEY DON'T GET IT!


Here is a list of a few of the most egregious examples of breed-specific health problems:

• Purine metabolism dysfunction gene in all (except pointer backcross) Dalmatians
• Protein malabsorption disorder in virtually all Norwegian Lundehunds ("Lundehund syndrome")
• Syringomyelia and Mitral valve disease in the vast majority of Cavalier King Charles Spaniels
• "Collie Eye Anomaly" in Collies and related breeds
• Copper toxicosis in Bedlington Terriers
• Fanconi Syndrome in Basenjis

Ah, but we can test and remove dogs with such bad genes from the genepool, right? Actually, that's how Fanconi syndrome became so prevalent in Basenjis. The Basenji breeders noticed a problem with hemolytic anemia. In attempting to eliminate hemolytic anemia, entire families of dogs were culled. Yes, the incidence of hemolytic anemia dropped, but they found many of their dogs were now afflicted with a fatal kidney disease, Fanconi syndrome. They had to return to Africa to add new stock to the decimated gene pool. 

And, according to geophysicist and canine genetics expert Sue Bowling:

“Unfortunately, we cannot breed animals based on a single gene – the genes come as a package. We may inbreed and rigorously remove pups with PRA or even their parents and littermates from the breeding pool. But remember inbreeding tends to make all genes more homozygous. In at least one breed, an effort to remove the PRA-causing gene resulted in the surfacing of a completely different and previously unsuspected health problem. It is easier and faster to lose genes (sometimes very desirable genes) from the breeding pool when inbreeding is practiced than when a more open breeding system is used. In other words, inbreeding will tend to produce more nearly homozygous animals, but generally some of the homozygous pairs will be "good" and others will be ‘bad’.....Furthermore, there may be genes where heterozygosity is an advantage……A more widespread case is the so-called major histocompatibility complex (MHC), a group of genes where heterozygosity seems to improve disease resistance.” (3)

Let's reduce it to something that even non-scientists can understand.

While health testing is admirable and a great beginning to a healthy future for dogs, no amount of health testing can substitute for outcrossing to produce robustly healthy dogs.

For the good of our breeds and all the dogs of the future, we need to change the current dog competition system. Conformation competition should be de-emphasized and standards need to be relaxed and more generalized. While today's dog shows do recognize and reward placid temperament, that is usually a secondary consideration to physical conformation characteristics.

If we want to improve the health of our breeds, the priority needs to be shifted to breeders who employ low levels of inbreeding; to those who breed first and foremost for excellence in temperament and ability as a worker or as a companion. Closed stud books need to be opened, and judicious crosses need to be allowed. Individual breed clubs need to invite outside genetics experts to help them develop policies to effectively manage their breed population.

The good work of AKC's Canine Health Foundation can and should be expanded. Beyond identifying genes that cause disease, the Foundation could employ geneticists for specific recommendations on how to better control genetic disease occurrence.

Our actions now will determine the ultimate fate of our dogs. Are you ready for the revolution?

(a) http://www.oregonlive.com/pets/index.ssf/2014/02/akc_hopes_to_clarify_common_mi.html
(1) http://www.veterinarypracticenews.com/vet-breaking-news/2013/06/04/study-shows-mutts-genetically-healthier.aspx
(2) http://www.ncbi.nlm.nih.gov/pubmed/23683021
(3) http://bowlingsite.mcf.com/genetics/inbreeding.html

Puff the Magic Hund Dog

Puff the Magic Hund Dog, lived by the sea
And frolicked in an autumn mist, in a land called Vaeroy!

Once upon a time, in land far away, lived a magical dog named "Puff."  He was born with six toes on each foot. Real, functional toes, not like the vestigial toes known as "dewclaws."

 

As he grew, his owner noticed that he was also quite magically double-jointed!

 

He had extra vertebrae in his neck.

Due to his unusual anatomy, Puff was able to climb steep cliffs and navigate rocky crags.

 

 

 He could flatten his ears completely, either backward and forward, which helped to keep out water or dirt.

His special talents came in handy for his job.....flushing puffin birds out from between the rocks, as well as retrieving puffin eggs from the nests. His flexible body and small size was perfect for maneuvering through caves, while his extra toes helped him to maintain a sure footing for climbing on rocks and scrambling along steep cliffs.

Puff and his relatives, who were all magically unique, flourished in Norway for hundreds of years. But, unfortunately for our Puffin Dog, known in Norway as the "Lunde Hund", it eventually became illegal to hunt puffins in Norway. He and his other family members no longer had a job, and soon, there were not many of them left. Then, distemper came along and wiped out almost all of the remaining dogs. There were less than a handful of Lundehunds left, and they were all closely related to each other.

Also unfortunate for the Lundehund is that, due to their lack of genetic variability, they are prone to a condition known as "Lundehund Syndrome." This syndrome is characterized by difficulty in digesting and absorbing protein. All Lundehunds suffer from this problem in varying degrees of severity. It can progress to cancer of the intestines or stomach or lymphoma.

http://lundehunds.com/lundehundsyndromeinfo.html

Is this genetic predisposition related to their strangely agile anatomy? We know in humans that being double-jointed is often a result of a genetic defect of collagen formation. I actually know someone with a protein malabsorption problem known as celiac disease, who cannot tolerate gluten in her diet, and she is also double-jointed. Some cases of celiac sprue are associated with abnormal collagen deposits in the intestines. It's interesting to speculate about the possible connection.

The Lundehund is closely related to the Icelandic Sheepdog and the Norwegian Buhund. "Lundies" are an attractive, moderate natural and somewhat primitive type of spitz dog, with the appearance of a cross between a wolf and a coyote.

I was lucky enough to see some of these unusual dogs up close and personal at the Eukanuba dog show a few years ago.

 At one time, I toyed with the idea of obtaining a "Lundie".  I thought it might be a good project to try to crossbreed with Buhunds in an attempt to reduce or eliminate the incidence of Lundehund syndrome. It's a serious problem that can result in significant pain and suffering, as well as a shortened lifespan. Whether caused by specific genes, or the result of lack of variability in the MHC (the genes that provide us with a healthy immune system), crossbreeding is the best way to introduce new genes that would help improve the overall health and vigor of the breed.

But now that AKC has "recognized" the Lundehund as a separate breed, it would be nearly impossible to undertake a crossbreeding program under the current closed registry system. "Purebred" being such an important attribute and all. Heaven forbid that we should MIX breeds, even though all through history people have done exactly that in order to produce healthy and functional dogs.

Incredibly, the genetic testing recommended for the Norwegian Lundehund  in AKC's CHIC program includes only OFA patella and CERF eye certification. 

Rather than admit there's a serious problem and look to fixing that problem, the Lundehund breeders justify their "pure" breeding by claiming that all breeds of dogs have different health problems. This is just their probem, they say, and that's just the way it is! No mention of crossing to similar breeds in an effort to produce healthier dogs.

I hope in the future that an adventurous breeder out there somewhere will undertake the important task of crossbreeding to truly IMPROVE the Norwegian Lundehund breed. The dogs of the future would thank us for that favor, and indeed, crossbreeding may be the only hope of for a bright future for these wonderful Lundies!