Tag Archives: genetics

Do breeders need to change?

The face of breeding, as I’ve known it, has changed considerably since I first joined the ranks of Gordon Setter breeders in the 70’s. So much more information is readily available, resources for every question can be found at the touch of a keyboard, cross-country breeding is accomplished without shuffling the bitch off to the airport, and the availability of genetic tests is growing quickly to theoretically help us breed healthier dogs. But are we, the breeders, utilizing the results of those tests with a consciousness that will improve the overall health of the breed or could misguided perception and dwindling numbers cause the downfall of the breed instead?

Photo by Susan Roy Nelson
Photo by Susan Roy Nelson “Four Ladies in a Row”

I just read, and then reread an article written by a Corgi breeder Joanna Kimball – “How We Must Change as Breeders and Why – A Football Field of Dogs”  published in Best In Show Daily (point and click on the bold title to link to the article). Joanna raised some valid points regarding breeding that I believe bear discussion among Gordon Setter breeders. I hope you’ll join me here in considering some of those points and then by sharing your own perceptions, agreements or disagreements as they be.

First the assumption that as a breeder we should all agree that only a very few dogs should ever be bred – is this true? The breeder’s thought process as Joanna wrote is “I should be as picky as possible, first health-test everybody, prove that each dog is healthy, make sure that only the ones who are incredibly high-quality in terms of conformation and show success are allowed to breed. I should build the next ten thousand dogs from the most elite pool of this one.” That’s the conventional wisdom, the way “good breeders” do everything, right?

In fact, Joanna says we should bear in mind thatEVERY DOG WHO IS REMOVED FROM THE POPULATION HURTS THAT POPULATION.” To maintain health in any breed we need to understand the need for genetic variation, and to retain genetic variation we need to be breeding from many lines, to many sires not only the one or two most popular sires and so on.

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Photo by Silvia Timmermann

I often want to go back to when I was younger, just starting out, and in this case I’m talking about the days when breeding wasn’t a four letter word and the propaganda of animal rights activists hadn’t put us all under their spell. The spell that makes breeders feel self-righteous for eliminating as many dogs as we can from the breeding pool because breeding is, after all, a very bad word. As the battery of DNA tests for genetic disorders continues to rise breeders are feeling satisfied as we believe we are gaining ground on health issues. But, should we also be considering that we might be losing ground on genetic diversity as we eliminate more and more dogs from the breeding pool with those tests?

Joanna states in another  point “SINCE EVERY DOG THAT IS REMOVED FROM THE POPULATION HURTS THE POPULATION, WE MUST REMOVE ONLY THOSE WHOSE PRESENCE WOULD HURT IT EVEN MORE.” To me this is like saying “Don’t throw the baby out with the bath water”. A common sense approach would include knowing what health condition could cause the death of our Gordon Setters, or what health condition would ruin the quality of life for our dogs, before making breeding choices based primarily on health testing, testing that if used incorrectly could eliminate other necessary qualities from the breed’s gene pool. Using testing to learn what, if any, health condition might be passed from one generation to the next is a wonderful tool, but it is not the only tool that a breeder should be using. Utilizing health testing to obtain the appropriate result in breeding requires very judicious application on the part of the breeder, who must also keep in mind the continued genetic diversity of the gene pool, as well as the overall soundness of the breed both physically and mentally.

Why, for example, would one choose to breed an OFA fair bitch to a dog because he had OFA good or excellent hips but also carried an unsound front, instead of breeding her to an OFA fair dog who is sound and beautifully moving both front and rear? In this case the breeder might get one or two additional puppies with better hip ratings (might) but the breeder will also be adding some puppies with those unsound fronts? Did the breeder really improve the breed or the gene pool with that breeding? Or, what about choosing to breed the Rcd4 carrier bitch to the Rcd4 clear dog whose parents both died of cancer at age 7, instead of breeding to the Rcd4 carrier dog whose parents died of old age at 13. We don’t have DNA tests for cancer available for Gordon Setters, but we do know that cancer causes the death of many Gordon Setters before their time, and we know the history of certain cancers can be prevalent in families. By theory, 25% of the puppies in the Rcd4 carrier to carrier litter could be affected, and at age 10 there may be one, perhaps even two of those affected dogs who might (there’s that word might again)  go blind from late onset PRA. Doesn’t the carrier to carrier litter – as a whole – have a better chance of living a healthy, happy life until old age takes them from us? Which choice does a breeder make and how does it affect the diversity of the gene pool? What if the breeder decides not to do either breeding because they don’t like the health choices? Can the diversity and size of the gene pool continue to be maintained if this were to be the constant decision?

Photo by Silvia Timmermann
Photo by Silvia Timmermann

So, why all this fuss about the gene pool, and gene pool diversity, and strength and size of the gene pool? A relatively simple example to help us understand is to look at the mixed breed population, and their reputation for being “healthier” than their purebred counterparts. Why is that? Genetic diversity is solidly at play. Odds are there are no common ancestors for generations in the pedigree of any mixed breed dog. A huge and diverse gene pool lies behind the mixed breed.

Before you decide I might be plumb crazy talking here about an issue with the size of gene pool let me ask you if you’ve read and absorbed, yes absorbed to the point where it makes perfect sense to you, the article at the Institute of Canine Biology by Carol Beachat PhD “Is your breed drifting?” (point and click on the bold printed title to link to this article)

As I look at the Gordon Setter in general, comparing them to other purebred dog breeds, I believe that Gordon Setters have relatively few genetic health issues that occur regularly. We are lucky in that respect. However, we cannot hope to improve the health characteristics we’d like to change, if our gene pool continues to shrink to the point where the majority of dogs are related, where there is not sufficient diversity to enact change. We need a diverse and a large population and we need responsible breeders who understand how to accomplish those health driven goals while maintaining the integrity of the breed.

by show ring
Photo by Bob Segal

As I look at dog show entries, where the rubber meets the road when it comes to proving the merit of our breeding stock, I find an ever decreasing number of Gordon Setter entries along with a decreasing number of new faces joining the ranks of breeders. Those who are showing today find ourselves scrambling to locate shows where there will be points, majors are difficult if not impossible to find unless sometimes you can bring your own entry – which accomplishes what exactly as far as improving the breed when you’ve finished a dog simply by winning over your own breeding? Specialties are struggling to build 5 point majors and many are no longer able to do so, despite offering two shows in one day. Our National Specialty entries have dropped from all time highs of between 450 to 550 dogs in ’93, ’94, and ’95 to approximately 220 entries for 2015, half the number that were participating 20 years ago.  Fewer entries, fewer breeders, fewer litters equals a smaller gene pool and thus loss of genetic diversity. To me this issue is two-fold; as breeders we need to appropriately and wisely utilize health testing without the elimination of too many dogs from the gene pool, and secondly we need to address the shrinking gene pool by understanding that we need to bring new breeder/exhibitors on to follow in our footsteps, to pick up the reins and drive on.

Many of you have been at this breeding/exhibiting thing for a while now. I’m curious how you feel about these concerns or better yet do you even believe there are such concerns? What would you change if you believe change is needed? How would you drive change? What do you think could be utilized to bring about improvement? Who do you believe is responsible for leading change in the breed? Can or should breeders accept responsibility for driving change?  How can breeders mentor others? So many questions and opinions, let’s start a discussion by sharing them, discussion is the first step. Your thoughts and comments are very welcome here, do remember to be respectful of others please.

For those of you who are Gordon owners but perhaps not involved in breeding and showing, what might entice you to change your focus, what would drive your interest in showing/breeding Gordon Setters? How would you want to learn? Who would you want to learn from? As above, your respectful thoughts and comments are welcome here.

To share your thoughts you may use the reply field at the very bottom of this article or click “Leave a Comment” at the very top of this article.

I’d like us to talk to each other people, as I believe change is needed and that is why I write this blog for you…to bring change through the sharing of information, common goals, and a love for our breed, the Gordon Setter.

Sally Gift, Mesa AZ

 References:

Part 2 – Do Breeders Need to Change?

Why all the fuss about inbreeding?

I’m sharing another great article from the Institute of Canine Biology with you today on breeding and genetics written by Carol Beuchat PhD.  This blog and Carol’s writings offer a wealth of information for the serious dog breeder and I’m going to be

Photo by Laurie Ward
Photo by Laurie Ward

recommending quite a bit of reading from this site for just that reason.

In this article Carol covers the topic of genetic disorders and the choices breeders face when planning a mating. She says “Breeders know that they can use inbreeding to concentrate the genes for the traits they prefer and to increase the predictability of a breeding by reducing variation in the offspring. But breeders have no way to increase the good genes but not the bad ones through inbreeding. (There are ways this can be done, but not using inbreeding.)”

As breeders we simply must take time to learn and understand genetics.  “You will hear people say that their lines are “healthy”, or that a particular problem is “not in my lines” This is a quote from Carol’s blog that I’ve heard oh, so very often, from many, many breeders over the years. Before you assume that you are safe to use statements like this as fact, read this article. It will indeed help you to more fully understand what lies beneath the surface.

Click the link that follows to be whisked away to the land of Genetics! Why all the fuss about inbreeding? (Or “Why are there so many genetic disorders in dogs?”) 

Sally Gift, Mesa AZ

Photo by Laurie Ward
Photo by Laurie Ward

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Food for thought… why can’t I get any puppies on the ground?

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Photo by Silvia Timmermann

I was talking with another breeder this week about the “state” of Gordon Setter litters, the quantity of litters being produced as well as size of the litters surviving. The conversation centered around the observation that overall, the Gordon Setter breed appears to be experiencing a decrease in fertility as well as in the viability of newborn offspring. Fewer breedings are taking, fewer puppies are surviving. As breeders I believe we all (yes, I include myself) need to hold ourselves responsible for understanding what may be causing the creation of fertility issues and for the creation of their solution. It’s been said many times by numerous authors before me, when choosing a breeding pair we must consider the fertility and nurturing qualities of the sire and dam in addition to every other trait we consider desirable. To do that, breeders need to understand pedigrees and how they speak to us about the inbreeding coefficient of the litter –  as that coefficient my friends, can drive what is known as “inbreeding depression.” To eradicate inbreeding depression we first need to learn how to identify it and when it appears we need to acknowledge that this could be at play and then we need to plan our breeding accordingly.

I’m not a geneticist and I won’t ever pretend to be, luckily though I am a voracious reader, and with all of the information at our fingertips on the internet today I can find a wealth of expert information for my own, as well as your reading pleasure. I urge you to explore with me, if you’ve not already done so.

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Photo by Silvia Timmerman

First let’s understand what’s meant by inbreeding. Inbreeding would be the breeding of related dogs who may be closely or distantly related to each other. Some, including me, designate inbreeding as close relationship breeding, like mother-son, father-daughter, sister-brother, and call “less close” breeding like a nephew-aunt breeding a line-breeding. But when reading articles written by the genetic expert you’ll find that it’s all packaged together under the name inbreeding. Don’t let that confuse you. With that said, if inbreeding is used carefully as part of a breeding plan that includes balancing the benefits with the dangers it can be a powerful tool. Using inbreeding without consideration of both positive and negative effects can be destructive.

Now let’s go back to inbreeding depression and talk about how that is related to the opening subject of decreased fertility in Gordon Setters and viability of newborn offspring. Inbreeding depression is not about an increase in the number of genetic disorders in the breed, like PRA for example. It refers to a loss of what a biologist would tell you is called fitness. Fitness in this context refers to the dog’s ability to pass on its genes to the next generation. So to a biologist, if a dog dies from disease before it can reproduce it has a fitness of zero. If a bitch successfully reproduces a litter but won’t properly care for her offspring (which will die without intervention) she has a fitness of zero. To breeders like us then, if our Gordon Setters have a high level of fitness they will produce offspring that can go on to reproduce themselves and perpetuate their genes in the population, where a Gordon Setter that cannot reproduce (without human intervention) or reproduces less effectively (below average litter size for example) have a low or zero fitness. In the Gordon Setter breed we could be experiencing evidence of inbreeding depression if we are in fact seeing an decrease in fertility and a decrease in litter viability. Evidence of inbreeding depression can be indicated by singleton litters, decline in conception rates, reduced sperm count, reduced litter size, lower pre and post-natal survival rates, shorter lifespans, higher cancer rates in young dogs, allergies, and many other issues that we might be taking for granted as normal in dog breeding these days. The “fitness” of the dog should be kept in mind as we make breeding choices.

My next step is to send you to some very informative articles I found at The Institute of Canine Biology (as I said earlier I am not a geneticist and won’t pretend that I can write in-depth articles about this topic). What a wonderful resource site!

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Photo by Silvia Timmermann

(Quick note – the photos included in this article are simply for your viewing pleasure, they have nothing to do with the content of the article).

Now, “don’t go throwing the baby out with the bathwater” my friends – that’s not the message here. Oh,and don’t forget to pass it on! Your comments, questions and suggestions are always encouraged in our comment section.

Sally Gift, Mesa, AZ

CHIC for DUMMIES – What is it – why should I use it?

This ought to be good – and yes that’s sarcasm!  I’m going to try to take all the long words and even longer sentences that describe CHIC (Canine Health Information Center) and boil them down to a few bullet points that briefly explain who, what, when, where, and how this thing works. To get a full explanation and a complete understanding of CHIC and it’s importance to the Gordon Setter you must read their home page for which I’ve supplied a link below.

WHO

WHAT

  • CHIC collects information about health issues (Gordon Setters).
  • CHIC gives advice about the health screening tests we (owners) need to do to improve the chances of Gordon Setters being born without those health issues.
  • CHIC keeps records of the dogs that are screened and a database of all those test results.
  • CHIC issues a number  when all screening tests are done on a dog – this number does not mean all tests were negative or clear.

WHEN

  • We (owners) screen or test Gordon Setters for the health issues CHIC told us about before breeding.
  •  We send our dog’s test results and DNA samples to the CHIC database and storage bank.
  • We send CHIC updated health information on our dog when a new or different issue comes up.

HOW

  • CHIC sends researchers our dog’s DNA when it’s needed for new research projects.
  • CHIC keeps parent club (owners) up to date on current health trends in the breed based on the data that we sent them.
  • Researchers find new answers to breeding healthy Gordon Setters.

And they all lived happily ever after…the End!

CHIC - breed health improvement plan

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Late-Onset (rcd-4) PRA in Gordon Setters

Thank you Jerold S. Bell for your permission to reprint this article.

Late-onset (rcd-4) progressive retinal atrophy in Gordon Setters:

Where are we, and where do we go from here?

Jerold S Bell DVM, Clinical Associate Professor of Genetics, Tufts Cummings School of Veterinary Medicine

(This article originally appeared in the August, 2011 TarTan Tidings)

Most owners have now received their rcd-4 PRA test results from the Animal Health Trust that were collected at the GSCA National Specialty in Ohio in June 2011. The AHT reports that of the 107 cheek swabs submitted from the collection; 3% test as affected (two copies of the defective gene), 30% test as carrier (one defective and one normal copy), and 67% test as clear (two normal copies of the gene).

The AHT previously reported a 50% carrier rate worldwide for the defective gene in Gordon Setters. However, this included all of the initial families of affected dogs that were used in the research to find the defective gene. The 30% carrier frequency from the dogs collected at the 2011 National probably represents a more accurate breed-wise US carrier frequency.

The rcd-4 gene that causes Gordon Setter PRA is one that similarly causes autosomal recessive late-onset progressive retinal atrophy in man. Owners of dogs who received affected test results are probably surprised with the result, and find no vision problems with their dogs. This is because this is a late-onset disorder. It was originally reported that the average onset of this form of PRA was around 10 years of age. This is the average age of Gordon Setters recognized with visual impairment that test affected with rcd-4 PRA. The actual age of onset of Gordon Setter rcd-4 PRA is possibly much older; with may affected dogs never reaching the age of onset of visual impairment. In addition, owners of very old Gordon Setters with visual impairment may believe that it is “normal” for old dogs to not see well, and do not pursue a diagnosis of PRA. The fact of the matter is that there is a range of age of onset for the clinical signs of Gordon Setter rcd-4 PRA where some may slowly lose their vision at younger than 10 years of age, and some may never show clinical signs of a vision problem.

Rcd-4 PRA is not the only inherited PRA in the breed. It has been shown that there is an earlier-onset PRA in the breed, with an average onset of 5 years of age. Some Gordon Setters clinically affected with this form of PRA and their parents have tested clear of the defective rcd-4 gene, proving that there are two separate genetic PRA disorders in the breed. Dr. Cathryn Mellersh at the AHT (cathryn.mellersh@aht.org.uk) is currently searching for the defective gene causing this form of PRA in the breed, and is interested in cheek swab samples from affected dogs and their close relatives.

Tucker driving Jeep (red flag)
Photo by Paul F. Doherty

Because there is more than one form of PRA in the breed, and because Gordon Setters can also have other disorders of the eyelids, cornea, lens, and retina, the rcd-4 genetic test does not replace the need for annual CERF examinations of the eyes. (since original publication of this article CERF is no longer operating see OFA website instead.) The most important thing that we need to do about rcd-4 PRA is to not devastate the Gordon Setter gene pool with widespread spaying/neutering, and the removing of quality dogs from breeding. Aside from the loss of quality dogs, the breed cannot withstand the removal of 30% of breeding dogs from the gene pool and maintain breed genetic diversity. This is the first direct gene test that is available for the breed, but it will not be the last. We must all recognize that the proper use of genetic tests for recessive disease is to breed quality carrier dogs to quality clear dogs, and replace the carrier parent with a clear-testing offspring that is of equal or better quality. If a quality dog that you determine deserves to be bred tests as a carrier, you certainly can and should breed the dog. You must make a decision counter to the emotional reaction when you received the carrier test result. Making a decision to not breed a quality dog based on a single testable gene is not appropriate. As long as carriers are not bred to carriers, no affected dogs will be produced. This is a testable and controllable gene. By dealing with rcd-4 PRA in an objective and informed manner, we can continue to produce quality Gordon Setters and work away from this single hereditary disorder. The goal is to slowly decrease the carrier frequency in the population and slowly replace carrier breeding stock with normal offspring. This will take many generations. A genetic test should not alter who gets bred, only who the dog gets bred to. For more information, please refer to the articles in the February TarTan Tidings (or the March, 2011 GSCA Newsletter).

Lastly, it is important to remember that this is about the dogs. We belong to a community that loves Gordon Setters. No one wants to produce carrier or affected dogs. The stigmatizing of breeders and quality dogs due to carrier status is an old, outdated and unacceptable practice. We need to be able to raise the level of conversation to constructive communication. We should all report rcd-4 test results on our dogs to the OFA open health databases. This includes clear, carrier, and affected dogs. An application form is available in the DNA tests section of the OFA website. The application should be mailed with a copy of the official test results from the Animal Health Trust. The fee for entering rcd-4 results into the OFA database is $15 for clear and carrier dogs, and is free for dogs testing affected. As more genetic tests become available, we will find that there are no “perfect” dogs. By working together we can improve our breeding attitudes, our breeding programs, and the overall health of the Gordon Setter breed.

(This article originally appeared in the August, 2011 TarTan Tidings)

(This article can be reprinted by permission of the author jerold.bell@tufts.edu)

Notes from the Editor

Additional links related to PRA:

About CERF:  After nearly 30 years of working towards the elimination of heritable eye disease in dogs, The Canine Eye Registration Foundation (CERF) is now closed.

(This article contains photos that are not intended nor do they relate to the content of the article.)

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Cerebellar Degeneration in the Gordon Setter

Thank you to Jerold Bell DVM for allowing us to reprint this article.

Jerold S Bell DVM, Tufts Cummings School of Veterinary Medicine, N. Grafton, MA USA

puppy by Silvia Timmerman
Photo by Silvia Timmermann

Cerebellar Degeneration CD (also referred to as Cerebellar Cortical Abiotrophy CCA, or Cerebellar Ataxia CA) is a hereditary neurological disease seen in the Gordon Setter breed, and caused by a simple autosomal recessive gene. It causes slowly progressive muscular in-coordination, with an onset or age of recognition of clinical signs between six months to four years of age. Pathology studies performed in the 1970’s show the onset closer to six months of age; but with mild clinical signs affected dogs may not be identified until later in life. CD is not related to the metabolic disorder lethal neonatal encephalopathy (DUNG’d) seen in 3 to 8 week old Gordon Setters.

The clinical signs of CD include: poor balance, frequent stumbling, a wide-based stance (feet planted far apart), a high-stepping gait, and head or body tremors. Affected dogs have normal mental alertness. Most affected dogs have a normal life expectancy, and pass away due to unrelated causes. There is no treatment for CD.

Drs. Alexander de Lahunta, Linda Cork, and Steven Steinberg published the clinical description and mode of inheritance of CD in the breed in the early 1908’s. In 2012, Dr. Natasha Olby at North Carolina State University identified the mutated gene. With autosomal recessive inheritance, both parent must be carriers of this mutated gene to produce affected offspring. Approximately one-quarter of offspring from such matings are expected to be affected; but statistical chance can cause none to several affected dogs in a litter. A genetic test is available for this mutated gene that will determine normal, carrier, or affected status. The test can be run at any age with cheek swabs, and costs $15 (US) per dog tested. (Submit DNA for Testing – NC State Veterinary Hospital).     (Link to form for submitting DNA for testing)

Gordon Setters affected with CD have been identified since a least the 1960s in both conformation and field trial lines throughout the United States, Canada, Europe, and Australia. Affected and carrier Gordon Setters worldwide do not “connect up” before generationally early ancestors of the breed. All confirmed affected Gordon Setters around the world have the identified mutated gene causing CD. This same mutation was identified in Dr. Olby’s laboratory to be the cause of CD in the Old English Sheepdog breed – showing a common ancestor as the original source of the mutation in both breeds. No other breeds have been identified with the same mutation to date.

Over the years, Gordon Setter breeders and owners have been surprised by a diagnosis of CD in their dogs, due to a lack of known relatives with the disorder. These occurrences are traditionally followed by more affected dogs from related lines. The ancestrally ancient origin of the mutated gene explains this occurrence. The mutated gene has been dispersed and propagated in the Gordon Setter breed since its origination. Now that there is an inexpensive and accurate genetic test for the mutated gene, ALL breedable Gordon Setters should be tested.

As with all testable simple autosomal recessive genes, quality carrier dogs can be bred to quality normal-testing mates. This prevents affected dogs from being produced. Quality normal-testing offspring should replace the carrier parent for breeding. Carrier offspring should be selected against for breeding homes. In this way, you have eliminated the single mutated gene, without losing the quality traits of the line. A genetic test for a simple recessive disorder should not change who gets bred, only who they get  bred to.

To assist breeders with health-conscious breeding, each dog’s results should be entered into the OFA Cerebellar Degeneration registry (OFA Form for submission of DNA). The test results will be listed on the dog’s OFA page. The cost is $15 per dog, $30 litter of 3 or more, and a kennel rate of $7.50 per dog if 5 or more dogs are entered by the same owner (all in $US). If a dog is out of two DNA tested clear Gordon Setter Parents, the OFA will provide a Clear by Parentage (CBP) certification. In this way, generations of Gordon Setters do not have to be tested.  CBP certification requires that both parents are CD tested and entered into the OFA registry, and that the parents and offspring have been DNA parentage certified (usually available through your national Kennel Club).

Cerebellar degeneration is not the most frequent genetic disorder affecting the breed, but is the oldest documented simple inherited disorder in Gordon Setters. With the availability of an accurate and inexpensive genetic test, no Gordon Setter, their owners or breeders should have to deal with the affected state of this disorder going forward.

(This article can be reprinted with permission from the author Jerold.bell@tufts.edu)

To order cheek swab kits by phone, call:
North Carolina State University Veterinary Genetics Laboratory
Phone-Voice Mail: 919.513.3314
Hours: Monday-Friday, 9 a.m. – 4 p.m.
Facility: NC State CVM Research Building

To order cheek swab kits via an e-mail at the following address:
vcgl@lists.ncsu.edu
Please state the following in your e-mail:
Your mailing address.
Number of kits you would like.
Type of test, (which breed), you are requesting,Gordon Setter, Cerebellar Degeneration.

Additional Links:  GSCA Health Survey 2004

(This article contains photos that are not intended nor do they relate to the content of the article.)

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The Kinked Tail – More Than It Appears

It’s not life threatening, it only happens occasionally, it doesn’t make them sick and it can easily be remedied with a quick and relatively painless surgery while they’re still babies. Sounds pretty harmless, nothing to be worried about or to take too seriously…or is it?

Photo by Bob Segal
Photo by Bob Segal

Over the years I’ve been privy to a few conversations among Gordon Setter people about puppies born with a kink in their tail. I once heard someone say that the puppy’s tail was kinked because it was a huge litter and the puppy was crowded in the uterus, so the tail didn’t have room to grow properly….really? Another time I heard it said that the bitch was crazy wild while she was pregnant and her rough-housing probably broke the tail before the pup was born and the tail healed wrong…uhmmm no.

So, understanding that there may be folks who don’t understand this phenomenon I thought I’d put a little something out here as food for thought. The best article on the topic that I’ve found so far was written by Ms MA J.H.C. Brooijmans-SchallenbergThe Kink in the Tail“.   “If we wish our pedigree dogs to have good futures, we will need to step up and take our collective responsibility for it.”  OLYMPUS DIGITAL CAMERAI’d advise you to read the article in full, I am not an expert and cannot be responsible for fully explaining everything in as much detail. I will only attempt a brief summary to get you started.

The tail is an extension of the spinal column, which consists of vertebrae that are built differently depending on their function. Congenital aberrations of the tail shape can be found in many animals including the dog, and these generally cause no issue as long as the defect is only found on the tail. The warning is that breeding these affected dogs can result in offspring with serious defects in other parts of the body.

Starting with the fertilized egg three germ layers are formed, the most important layer, the Mesoderm is where the entire skeleton (excluding the crown of the skull), the heart, the blood vessels and the urogenital system are shaped. In the early stages of the embryonic development a great number of genetic factors pass on their information. Mutations occur often, and when they occur in the reproductive cells the changes are transferable to descendents.

As a result, there are many things (other than simply a kinked tail) that could be transferred to the offspring if Gordon Setters with kinked tails are used in breeding, and this is due to the formation of not only the skeleton, but also the heart, blood vessels and urogenital systems in the same layer, the Mesoderm. For example the offspring could have defects in the spinal column or any other part of the skeleton and jaw. Perhaps the defect could be an aortic atrium septum (undersized septum in the heart) or aortic stenosis (aorta too narrow in places), or the embryonic blood vessels fail to disappear after birth. Another defect could occur involving urethra running from kidney to bladder that is not implanted in the bladder past the sphincter. Females with this abnormality often display incontinent behavior. Males have two sphincters so this defect could be present but not evident. This is a very short list of the many abnormalities that can occur.

The Gordon Setter Health Survey conducted in 2004 for the Gordon Setter Club of America Inc. reported that 6.06% of the total population survey reported Kinked Tails under Musculoskeletal health problems. Certainly not a huge portion of the population but it does indicate to us as breeders that this occurs in the Gordon Setter. As breeders, I hope I’ve helped you gain a better understanding of what could be at play and the risk. I do hope our readers  and others who may be much more expert on this topic than I, will share your thoughts, additions or additional information in the comment section below!

Sally Gift, Mesa AZ

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The Genetics of Bloat | Tufts Now

Bloat, just the mention of the word sends shivers down my spine and a knot straight to my gut.  As Gordon Setter owners and breeders I’m guessing many of you have a similar response. Yes, we own one of those deep-chested breeds with a propensity to bloat that keeps us on our toes learning the latest methods to treat or avoid it as well as following the most recent research.

We’re providing you with a link today to an article appearing on Tufts Now “The Genetics of Bloat” By Genevieve Rajewski that discusses a research project taking place  this year.”Researchers hope their work will help predict which dogs may get the deadly disease.”

See more at: The Genetics of Bloat – Tufts Now

Additional Links:  GSCA Health Survey 2004 Results

Books about breeding that are not X-rated!

Once I was young, naive and considered crazy by my family. Well, actually my family considered me crazy for a number of reasons, but to stay on topic the one I’m referring to here was my desire to breed show dogs, Gordon Setter show dogs to be exact. What was I thinking?

I digress, you see what I wanted to share with you today was the book that became my “dog breeding bible” way back when we all “walked a mile to school, barefoot through the snow”. And, if you’re too young to have heard your parents (or grandparents for some of you) say that, you’re probably too young to be witnessing sex between dogs so perhaps you should skip on out of here.

Back in 1980 a fine lady by the name of Ann Serrane authored this fantastic book called “The Joy of Breeding your own Show Dog”. I read that book from cover to cover so many times I’ve memorized whole chapters. I kept that book next to the whelping box every time I had a litter (no, you don’t want to know what the stains were from on some of the pages). Ann’s book starts at the beginning, before you’ve bred the bitch, and covers everything from simple genetics and pedigrees through whelping the puppies and caring for fragile newborns. Ann taught me so many things, like the importance of knowing the traits of the dogs in the pedigree to other life saving things like using a glucose solution to rehydrate newborns to keep them strong so they could nurse. She taught me when to call the vet and what that vet would really need to know. (Told you I memorized whole chapters!)

Joy of Breeding Show dog

I’ve read several other books about breeding dogs, but they just weren’t as useful to me, some were missing information that Anne had included, others were not as clearly written, and very few offered me new ideas or concepts.  I don’t know, must have been a first love sort of thing, but no book ever quite replaced this one for me.

There was a reprint of this book and I’ve found used copies online, I’ve seen it at dog shows and have even found a site where it can be downloaded – though I’m not seeing the fun in having an electronic copy that can’t be left around for a few puppies to chew.

So, now that I’ve gotten that off my chest how about you all share with us!

What’s your favorite book about breeding dogs? Do you have one? Who wrote it and why did you use it?

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