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What is my puppy eating?

Your puppy is eating  Purina Pro Plan puppy food. Your puppy  should be fed three times a day. Morning, Afternoon & Evening. For best Potty training results do not feed after 7 pm.


Unlike people, who can eat a variety of foods in a single day and not have any digestive upset, your dog’s digestive system is much more sensitive.

On average, your dog will need a seven-day transition period when switching to a new food. If you change his food too quickly, you may find your pet from becoming sick, which will involve a messy cleanup for you.

Although the average amount of time it will take for you to switch your dog’s food is a week, it may take some dogs longer to become completely accustomed to the new chow.

For example, if you are currently feeding a kibble that is high in grain and corn, like Pedigree or Hill’s Science Diet, and you want to switch to a more natural grain-free dog food — like Nature’s Variety Instinct, Taste of the Wild or Natural Balance LID — the extreme ingredient differences between the two types of food may cause the transition period to be longer.

The following is a good set of guidelines for transitioning your dog between two foods with similar ingredient panels.

Transitioning to a Different Dog Food, Gradually

  • Days      1-2: During      the first couple of days of starting a new food, mix 75 percent      old with 25 percent new food. You want to feed these two      together, not separated. Examine the feeding guidelines on the new bag of      food — overfeeding is the top reason dogs are overweight.
  • Days      3-4: If      you notice that your dog has loose stools or an upset stomach after the      first two days, continue to feed less of the new stuff before increasing      the percentage. If your dog has diarrhea or loose stools, along with      slowing the transition, adding a small amount of canned pumpkin in the      diet may help firm up the stools again. (Oddly enough, pumpkin can act as      both stool firmer and softener.) In the case      that he seems to be okay, change the percentage to 50 percent old      and 50 percent new.
  • Days      5-6: At      this point, you can change the percentage to 25 percent old and 75      percent new. Always look for signs of an upset stomach so you can      slow the transition if needed.
  • Day      7: You      can now start feeding your dog 100 percent of the new dog      food.

Best Food Hands down to feed your puppy is a balanced raw food diet. However that is not always feasible so please choose a food with less fillers and more meat. 

Do's, Dont's & Common Q&A's

  

Please DO NOT take your puppy to heavily trafficked areas until he/she has had their full course of vaccinations, including rabies at the age of 16 weeks.


DO Follow up vaccinations when your puppy is 11 weeks & 15 weeks. Rabies Vaccination at 16 weeks. 


DO Remember your puppy is still growing.  He/She will need lots of sleep. Like a human child they can get cranky when tired and/or hungry. 


Please be mindful of your puppies exercise. DON'T overdo it. 


Please DO  talk with your veterinarian on age appropriate exercise. 

 

For emergencies always contact your veterinarian.


PLEASE DO NOT FEED YOUR PUPPY GRAIN FREE FOOD


Is my puppy microchipped?

Yes. Your puppy is micro chipped with AKC Reunite micro chips. 


Do you do health checks on puppies?

Yes. Your Puppy will have a veterinarian health visit between 6 & 7 weeks of age. 


Has my puppy had age appropriate dewormings & vaccinations?

Yes. Your puppy is de-wormed at 2,4,5,6,7 & 8 weeks old. Your puppy will have his/her first vaccination at 7 weeks. 

After bringing puppy home. Please also take him/her to your vet for a NEW WELL PUPPY EXAM.


My puppy is an ICH Carrier. What does that mean?

         That means he/she carries a copy of that gene. He/She will have no symptoms or problems associated with ichtyosis. Puppy would have to have the affected gene to be symptomatic.


How often should I feed my puppy?

Your puppy should be fed no less than 3 times a day(Morning, Afternoon & Evening) You can decrease to 2 feedings per day at around 4 to 5 months of age. For best potty training results           Do Not feed after 7 pm. 


Potty training tips-

Always take to the same spot outside for potty.

Generally 20 mins to 30 mins after eating/drinking take outside for potty and again right before bedtime. 

When accidents occur in the house NEVER spank or rub your puppies nose in their accident. Always clean up area. Tell your puppy NO (Firmly but gently). Then place soiled cleaning material in outside potty area, let your puppy sniff and then praise them.  It won't take long before they understand what you are asking. (Be mindful of their cues. Whining. Circling. Scratching at the door. After eating/drinking. Ect.


Do you crate train?

I do not. Some crate training tips 

(from the AKC website) 

 

Choose a well-ventilated crate that is large enough for your puppy to stand up, lie down, and turn around. Remember that your puppy’s crate will have to grow as he does, so purchase a crate that is appropriate for your dog’s expected full-grown size, and use a divider to make the crate smaller for the time being. Many crates available at pet-supply stores include dividers.

Why size matters: A crate that’s too small will be uncomfortable for your dog, but a crate that’s too large may give your dog the space he needs to have an accident without it ruining his bedding. This behavior might encourage future accidents in the crate and around the home.  

The most important part of crate training is making sure your puppy always associates it with a positive experience.

Start by lining it with blankets and place a few toys inside to make it cozy. You can also cover it with a lightweight blanket to mimic a “den” environment. Make sure it is still ventilated and not too hot if you do this.

Bring your puppy to the crate for naps and quiet-time breaks so that he can “unwind” from family chaos. Start in increments of 10 minutes and work up to longer periods. Offer treats when he goes inside, and distraction toys, like a stuffed KONG.

 

Every time you take the puppy out of the crate, take him for a walk so he can eliminate. He’ll get used to the idea that potty time comes after crate time. Remember to praise him after he goes to the bathroom outside.

It’s also helpful to keep puppies in the crate overnight. They may cry the first night or two—in most cases, they are simply adjusting to home without their mom and littermates. Most puppies should be able to sleep through the night without a potty break by 4 months of age, but if you’re in doubt, take him outside.

 

Never leave a puppy in his crate all day; he needs several bathroom breaks, as well as playand feeding times. Even though he won’t want to soil his sleeping area, if he is in there for extremely long stretches, he just might. (He can’t help it!) And if he does, it is because his owner has neglected his responsibility, not because the dog has misbehaved.

Never use the crate as punishment. Your dog should see his “room” as a place where only happy, peaceful things happen.

Never lose your patience. Learning takes time. If you follow the above advice and are consistent, your puppy will learn to love his crate for years to come

AKC-Expert Advice from training to health

PennHip vs OFA

  

Research has shown that the heritability (the passing of a trait to offspring) is much higher for the distraction index (DI) that tells the laxity of a hip joint. In contrast, scoring of the two-year old dog by simply looking at joint conformation and the presence or absence of osteoarthritis (i.e. having an OFA done) has not shown to be predictably passed on. This is why there is no guarantee that if you breed OFA graded "excellent" dogs to each other that you'll get OFA graded "excellent" puppies.

It is also why you can't take an OFA "excellent" dog, breed it to an OFA "fair" dog, and get OFA "good" (meaning a grading somewhere in between) puppies. The heritability simply doesn't work that way.

Again, on the other hand, the high heritability of the PennHIP does allow for choosing breeding pairs that can move the average DI through successive litters toward a better and better score. Of course, ideally you breed only dogs with very low DI measurements period. But sometimes that is not how the real world works. PennHIP allows you the ability to know which dogs need to be bred, which don't, and which ones will need help by only being bred to other very tight hipped (low DI) dogs.


Study compares PennHIP vs OFA hip dysplasia tests

Ben Williams

Responsible breeders are always trying to reduce the risk of hip dysplasia in their dogs blood lines. One way to achieving this goal is to have an accurate test for susceptibility to this disease. A recent study attempted to look at the differences in the two most common tests.

Currently the test regarded as the "gold standard" used to determine a dogs susceptibility to hip dysplasia is the Orthopedic Foundation for Animals (OFA) hip joint scoring system. This system rates a dogs hip joint on a seven-point scoring system. The test relies on interpretation of a radiograph of the dogs hips, which are then assigned a score by three independent radiologists: Excellent, Good, Fair, Borderline, Mild, Moderate and Severe 

Another, more recently developed test, is the University of Pennsylvania Hip Improvement Program(PennHIP) test. Unlike the OFA test, PennHIP requires the dog to be anesthetized. Three radiographs are taken to measure the hip joint laxity. A score between 0-1 is assigned, with 0 being very tight hips and 1 being very loose. The test is not pass-fail, and the score is actually based on a measurement of the hip’s distraction index (DI).

According to the organization, "the DI is an indication of the ‘percent out of joint’ that the femoral head is displaced from the acetabulum." So a DI of 0.15 means the femoral head is 15 percent out of joint (a tight hip), and a DI of 0.77 means the head is 77 percent out of joint (a pretty loose hip). The index is measured using circular gauges that are placed over the films, and the final number reflects factors such as the size of the dog and how it compares to the rest of the population. This method generally defines a DI of ≥0.30 as "osteoarthritis-susceptible," and a DI of ≤0.30 as "osteoarthritis-non-susceptible."


A recent study compared the relationship between the OFA hip joint scores and the PennHIP distraction index values.

The study was conducted by researchers from the University of Pennsylvania’s School of Veterinary Medicine, one of whom, Gail Smith, VMD, PhD, invented the PennHIP method. The study found that the PennHIP method was a more accurate indicator of dogs’ susceptibility to osteoarthritis.

"Results suggested that OFA scoring of HE [hip joint-extended] radiographs underestimated susceptibility to osteoarthritis in dogs, which may impede progress in reducing or eliminating hip dysplasia through breeding," the study says.

The researchers looked at the differences in the OFA scores and the PennHIP DIs of radiographs of 439 dogs that were screened between 1987 and 2008. The specific results showed that:

  • 14% of dogs had hip joints scored as excellent by OFA standards, but 52% (31/60) of those had a DI ≥0.30 (range, 0.14 to 0.61)
  • 82% of dogs with OFA-rated good hip joints had a DI ≥0.30 (range, 0.10 to 0.77)
  • 94% of dogs with OFA-rated fair hip joints had a DI ≥0.30 (range, 0.14 to 0.77)
  • Of all dogs with fair to excellent hip joints by OFA standards, 80% had a DI ≥0.30.
  • All dogs with OFA-rated borderline hip joints or mild, moderate, or severe hip dysplasia had a DI ≥0.30 (range, 0.30 to 0.83).

Specialist weighs in
Reproductive specialist Milan Hess, DVM, DACT, of Colorado Veterinary Specialists said her clinic performs OFA tests more often than PennHIP.

"Breeders know what Excellent, Good or Fair means when discussing hip scores," Hess said. "Breeders are typically not educated in distraction indices or in knowing how their dogs hips compared to the rest of the population can help them make objective breeding choices. OFA evaluation does not require heavy sedation or general anesthesia and requires only one view. For these reasons, OFA evaluation is significantly less expensive than PennHIP evaluation. OFA does not require films to be submitted so breeders can elect not to submit films with obviously poor joint conformation. Finally, OFA evaluations tend to be easier to ‘pass’ than PennHip evaluations and many breeders are unfortunately more interested in passing the test than having an objective evaluation in which the result may not be as good."

While the conclusions of the study may seem foregone, Hess said the results published generally correlate with her experience with the two methods. However, she pointed out that the lack of improvement in dogs’ hips is not only the fault of the evaluation method.

"As veterinarians, we need to encourage owners to submit films that will obviously not pass due to poor joint conformation AND make the results available to the public (there is a box on the OFA form the owner can initial if they wish to have non-passing results made public)," Hess said. "It does no good for a breeder to be using a dog with Excellent hips if they didnt know that 3 of the littermates were dysplastic. Used properly, OFA evaluations likely could be used to direct selection pressure to improve hip scores."

The study, "Evaluation of the relationship between Orthopedic Foundation for Animals’ hip joint scores and PennHIP distraction index values in dogs," was published in the Journal of the American Veterinary Medical Association (JAVMA) in September 


DNA Test Results Explained

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Progressive Retinal Atrophy, Progressive Rod-Cone Degeneration

 Other Names:PRA-PRCD, PRCDAffected Genes:PRCDInheritance:Autosomal RecessiveMutation:Point Mutation

Common Symptoms

Progressive retinal Atrophy, progressive Rod-cone degeneration (PRA-prcd) is a late onset, inherited eye disease affecting Golden Retrievers. PRA-prcd occurs as a result of degeneration of both rod and cone type Photoreceptor Cells of the Retina, which are important for vision in dim and bright light, respectively. Evidence of retinal disease in affected dogs can first be seen on an Electroretinogram around 1.5 years of age for most breeds, but most affected Golden Retrievers will not show signs of vision loss until 5 to 6 years of age or later. The rod type cells are affected first and affected dogs will initially have vision deficits in dim light (night blindness) and loss of peripheral vision. Over time affected dogs continue to lose night vision and begin to show visual deficits in bright light. Other signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the retina called the Tapetum that can be observed on a veterinary eye exam. Although there is individual and breed variation in the age of onset and the rate of disease progression, the disease eventually progresses to complete blindness in most dogs. Other inherited disorders of the eye can appear similar to PRA-prcd. Genetic testing may help clarify if a dog is affected with PRA-prcd or another inherited condition of the eye.

Breed-Specific Information for the Golden Retriever

The Mutation of the PRCD gene associated with progressive retinal Atrophy, progressive Rod-cone degeneration has been identified in Golden Retrievers, although its overall frequency in this breed is unknown.

Testing Tips

Genetic testing of the PRCD gene in Golden Retrievers will reliably determine whether a dog is a genetic Carrier of PRA-prcd. PRA-prcd is inherited in an Autosomal Recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. In general, carrier dogs do not have features of the disease but when bred with another carrier of the same Mutation, there is a risk of having affected pups. Each pup that is born to this pairing has a 25% chance of inheriting the disease and a 50% chance of being a carrier of the PRCD gene mutation. Reliable genetic testing is important for determining breeding practices. Because symptoms do not appear until adulthood, genetic testing should be performed before breeding. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers to each other is not recommended. Golden Retrievers that are not carriers of the mutation have no increased risk of having affected pups. However, because there are multiple types of PRA caused by mutations in other genes, a normal result in PRCD does not exclude PRA in a pedigree.

There may be other causes of this condition in dogs and a normal result does not exclude a different mutation in this gene or any other gene that may result in a similar genetic disease or trait.

References

  • Dostal J, Hrdlicova A, Horak P. Progressive rod-cone degeneration (PRCD) in selected dog breeds and variability in its phenotypic expression. Veterinarni Medicina. 2011 Jun; 56(5):243-47. [Not In PubMed]
  • Kohyama M1, Tada N, Mitsui H, Tomioka H, Tsutsui T, Yabuki A, Rahman MM, Kushida K, Mizukami K, Yamato O. Real-time PCR genotyping assay for canine progressive rod-cone degeneration and mutant allele frequency in Toy Poodles, Chihuahuas and Miniature Dachshunds in Japan. J Vet Med Sci. 2015 Nov 6. [PubMed: 26549343]
  • Moody JA, Famula TR, Sampson RC, Murphy KE. Identification of microsatellite markers linked progressive retinal atrophy in American Eskimo Dogs. Am J Vet Res. 2005 Nov;66(11):1900-2. [PubMed: 16334947]
  • Zangerl B, Goldstein O, Philp AR, Lindauer SJ, Pearce-Kelling SE, Mullins RF, Graphodatsky AS, Ripoll D, Felix JS, Stone EM, Acland GM, Aguirre GD. Identical mutation in a novel retinal gene causes progressive rod-cone degeneration in dogs and retinitis pigmentosa in humans. Genomics. 2006 Nov; 88(5):551-63. [PubMed: 16938425]

Progressive Retinal Atrophy, Golden Retriever 1-Results-Clear

 Other Names:GR-PRA1, GR1-PRA Genes:SLC4A3Inheritance:Autosomal RecessiveMutation:Insertion


Common Symptoms

Progressive retinal Atrophy, golden retriever 1 (GR-PRA1) is a late-onset inherited eye disease affecting golden retrievers. Affected dogs begin showing clinical symptoms related to retinal degeneration between 6 to 7 years of age on average, though age of onset can vary. Initial clinical signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the Retina called the Tapetum that can be observed on a veterinary eye exam. Progression of the disease leads to thinning of the retinal blood vessels, signifying decreased blood flow to the retina. Affected dogs initially have vision loss in dim light (night blindness) and loss of peripheral vision, eventually progressing to complete blindness in most affected dogs.

Breed-Specific Information for the Golden Retriever

The Mutation of the SLC4A3 gene associated with progressive retinal Atrophy, golden retriever 1 has been identified in golden retrievers. Though the frequency in the overall golden retriever population is unknown, in one study of 369 golden retrievers clinically free of disease tested from the UK, US, Sweden, and France, 10.5% were carriers of the mutation.

Testing Tips

Genetic testing of the SLC4A3 gene in golden retrievers will reliably determine whether a dog is a genetic Carrier of GR-PRA1. GR-PRA1 is inherited in an Autosomal Recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. In general, carrier dogs do not have features of the disease but when bred with another carrier of the same Mutation, there is a risk of having affected pups. Each pup that is born to this pairing has a 25% chance of inheriting the disease and a 50% chance of inheriting one copy and being a carrier of the SLC4A3 gene mutation. Reliable genetic testing is important for determining breeding practices. Because symptoms do not appear until adulthood, genetic testing should be performed before breeding. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers to each other is not recommended. Golden retrievers that are not found to have this specific mutation have no increased risk of having affected pups for progressive retinal Atrophy, golden retriever 1. However, because there are multiple types of progressive retinal atrophy caused by mutations in other genes, a normal result in SLC4A3 does not exclude progressive retinal atrophy in a pedigree.

There may be other causes of this condition in dogs and a normal result does not exclude a different mutation in this gene or any other gene that may result in a similar genetic disease or trait.

References

  • Downs LM, Wallin-Hakansson B, Boursnell M, Marklund S, Hedhammar A, Truve K, Hubinette L, Lindblad-Toh K, Bergstrom T, Mellersh CS. A frameshift mutation in golden retriever dogs with progressive retinal atrophy endorses SLC4A3 as a candidate gene for human retinal degenerations. PLoS One. 2011;6(6):e21452. [PubMed: 21738669]

Progressive Retinal Atrophy, Golden Retriever 2

 Other Names:GR-PRA2, GR2-PRA

Genes:TTC8Inheritance:Autosomal RecessiveMutation:Deletion

Common Symptoms

Progressive retinal Atrophy, golden retriever 2 (GR-PRA2) is a late-onset inherited eye disease affecting golden retrievers. Affected dogs begin showing clinical symptoms related to retinal degeneration at around 4 to 5 years of age on average, though age of onset can vary. Initial clinical signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the Retina called the Tapetum that can be observed on a veterinary eye exam. Progression of the disease leads to thinning of the retinal blood vessels, signifying decreased blood flow to the retina. Affected dogs initially have vision loss in dim light (night blindness) and loss of peripheral vision, progressing to complete blindness in most affected dogs.

Breed-Specific Information for the Golden Retriever

The Mutation of the TTC8 gene associated with GR-PRA2 has been identified in golden retrievers. Though the frequency in the overall golden retriever population is unknown, in one study of golden retrievers either free of clinical disease or of unknown PRA status tested from the UK, US, France, and Sweden, 3% were carriers of the mutation.

Testing Tips

Genetic testing of the TTC8 gene in golden retrievers will reliably determine whether a dog is a genetic Carrierof GR-PRA2. GR-PRA2 is inherited in an Autosomal Recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. In general, carrier dogs do not have features of the disease but when bred with another carrier of the same Mutation, there is a risk of having affected pups. Each pup that is born to this pairing has a 25% chance of inheriting the disease and a 50% chance of inheriting one copy and being a carrier of the TTC8 gene mutation. Reliable genetic testing is important for determining breeding practices. Because symptoms do not appear until adulthood, genetic testing should be performed before breeding. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers to each other is not recommended. Golden retrievers that are not found to have this specific mutation have no increased risk of having affected pups. However, because there are multiple types of progressive retinal Atrophycaused by mutations in other genes, a normal result in TTC8 does not exclude progressive retinal atrophy in a pedigree.

There may be other causes of this condition in dogs and a normal result does not exclude a different mutation in this gene or any other gene that may result in a similar genetic disease or trait.

References

  • Downs LM, Hitti R, Pregnolato S, Mellersh CS. Genetic screening for PRA-associated mutations in multiple dog breeds shows that PRA is heterogeneous within and between breeds. Vet Ophthalmol. 2014 Mar;17(2):126-30. doi: 10.1111/vop.12122. Epub 2013 Nov 21. [PubMed: 24255994

Ichthyosis (Golden Retriever Type)

 Affected Genes:PNPLA1Inheritance:Autosomal Recessive With Variable ExpressivityMutation:Complex Rearrangement


Common Symptoms

Ichthyosis (golden retriever type) is an inherited condition of the skin affecting golden retrievers. The age of onset and severity of disease are highly variable, however most affected dogs present before one year of age with flaky skin and dull hair. Over time the skin develops a grayish color and appears thick and scaly, especially over the abdomen. The symptoms may progress to severe scaling all over the body, may improve with age, or may come and go over the dog’s lifetime. While the prognosis is generally good for affected dogs, they are at increased risk for skin infections.

Breed-Specific Information for the Golden Retriever

The Mutation of the PNPLA1 gene associated with Ichthyosis (golden retriever type) has been identified in the golden retriever. Though the exact frequency in the overall golden retriever population is unknown, approximately 44% out of 1600 golden retrievers tested from Australia, France, Switzerland, and the United States were carriers of the mutation and approximately 29% were affected.

Testing Tips

Genetic testing of the PNPLA1 gene in golden retrievers will reliably determine whether a dog is a genetic Carrier of Ichthyosis (golden retriever type). Ichthyosis (golden retriever type) is inherited in an Autosomal Recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. In general, carrier dogs do not have features of the disease but when bred with another carrier of the same Mutation, there is a risk of having affected pups. Each pup that is born to this pairing has a 25% chance of inheriting the disease and a 50% chance of inheriting one copy and being a carrier of the PNPLA1 gene mutation. Reliable genetic testing is important for determining breeding practices. Because some affected dogs exhibit very mild symptoms, genetic testing should be performed before breeding. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers to each other is not recommended. Golden retrievers that are not carriers of the mutation have no increased risk of having affected pups.

There may be other causes of this condition in dogs and a normal result does not exclude a different mutation in this gene or any other gene that may result in a similar genetic disease or trait.

References

  • Grall A, Guaguère E, Planchais S, Grond S, Bourrat E, Hausser I, Hitte C, Le Gallo, M., Derbois C, Kim GJ, Lagoutte L, Degorce-Rubiales F, Radner FP, Thomas A, Küry S, Bensignor E, Fontaine J, Pin D, Zimmermann R, Zechner R, Lathrop M, Galibert F, André C, Fischer J. PNPLA1 mutations cause autosomal recessive congenital ichthyosis in golden retriever dogs and humans. Nat Genet. 2012 Jan 15;44(2):140-7. [PubMed: 22246504]
  • Guaguere E, Bensignor E, Küry S, Degorce-Rubiales F, Muller A, Herbin L, Fontaine J, André C. Clinical, histopathological and genetic data of ichthyosis in the golden retriever: a prospective study. J Small Anim Pract. 2009 May;50(5):227-35. [PubMed: 19413748]
  • Guaguere E, Thomas A, Grall, A, Bourrat E, Lagoutte L, Degorce-Rubiales F, Hitte C, Bensignor E, Fontaine J, Pin D, Queney G, Andre C. Autosomal recessive ichthyosis in golden retriever dogs: distribution and frequency of the PNPLA1 mutant allele in different populations. In Torres SMF, Fran LA, Hargis AM. Ames (eds), Advances in Veterinary Dermatology, 7th ed. John Wiley & Sons Ltd, 2013.

Degenerative Myelopathy

 Other Names:Canine degenerative myelopathy, DM Genes:SOD1Inheritance:Autosomal RecessiveWith Incomplete PenetranceMutation:Point Mutation


Common Symptoms

Degenerative Myelopathy caused by Mutation of the SOD1 gene is an inherited neurologic disorder of dogs. This mutation is found in many breeds of dog, including the golden retriever. While it is not clear for some of the other breeds, golden retrievers are known to develop degenerative myelopathy associated with this mutation. The variable presentation between breeds suggests that there are environmental or other genetic factors responsible for modifying disease expression. The average age of onset for dogs with degenerative myelopathy is approximately nine years of age. The disease affects the White Matter tissue of the spinal cord and is considered the canine equivalent to amyotrophic lateral sclerosis (Lou Gehrig’s disease) found in humans. Affected dogs usually present in adulthood with gradual muscle Atrophy and loss of coordination typically beginning in the hind limbs due to degeneration of the nerves. The condition is not typically painful for the dog, but will progress until the dog is no longer able to walk. The gait of dogs affected with degenerative myelopathy can be difficult to distinguish from the gait of dogs with hip dysplasia, arthritis of other joints of the hind limbs, or intervertebral disc disease. Late in the progression of disease, dogs may lose fecal and urinary continence and the forelimbs may be affected. Affected dogs may fully lose the ability to walk 6 months to 2 years after the onset of symptoms. Affected medium to large breed dogs, such as the golden retriever, can be difficult to manage and owners often elect euthanasia when their dog can no longer support weight in the hind limbs.

Breed-Specific Information for the Golden Retriever

The Mutation of the SOD1 gene associated with degenerative myelopathy has been identified in the golden retriever. The overall frequency of this disease is unreported for golden retrievers. However, in one study of 334 golden retrievers tested, 0.6% were carriers of the mutation and 3% were at-risk/affected.

Testing Tips

Genetic testing of the SOD1 gene in golden retrievers will reliably determine whether a dog is a genetic Carrierof degenerative myelopathy. Degenerative Myelopathy is inherited in an Autosomal Recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. In general, carrier dogs do not have features of the disease but when bred with another carrier of the same Mutation, there is a risk of having affected pups. Each pup that is born to this pairing has a 25% chance of inheriting the disease and a 50% chance of inheriting one copy and being a carrier of the SOD1 gene mutation. Reliable genetic testing is important for determining breeding practices. Because symptoms may not appear until adulthood and some at-risk/affected dogs do not develop the disease, genetic testing should be performed before breeding. Until the exact modifying environmental or genetic factor is determined, genetic testing remains the only reliable way to detect neurological disease associated with this mutation prior to death. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers to each other is not recommended. Golden retrievers that are not carriers of the mutation have no increased risk of having affected pups.

There may be other causes of this condition in dogs and a normal result does not exclude a different mutation in this gene or any other gene that may result in a similar genetic disease or trait.

References

  • Awano T, Johnson GS, Wade CM, Katz ML, Johnson GC, Taylor JF, Perloski M, Biagi T, Baranowska I, Long S, March PA, Olby NJ, Shelton GD, Khan S, O'Brien DP, Lindblad-Toh K, Coates JR. Genome-wide association analysis reveals a SOD1 mutation in canine degenerative myelopathy that resembles amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A. 2009 Feb 24; 106(8):2794-9. [PubMed: 19188595]
  • Coates JR, March PA, Oglesbee M, Ruaux CG, Olby NJ, Berghaus RD, O'Brien DP, Keating JH, Johnson GS, Williams DA. Clinical characterization of a familial degenerative myelopathy in Pembroke Welsh Corgi dogs. J Vet Intern Med. 2007 Nov-Dec; 21(6):1323-31. [PubMed: 18196743]
  • Coates JR, Wininger FA. Canine degenerative myelopathy. Vet Clin North Am Small Anim Pract. 2010 Sep; 40(5):929-50. [PubMed: 20732599]
  • Miller AD, Barber R, Porter BF, Peters RM, Kent M, Platt SR, Schatzberg SJ. Degenerative myelopathy in two Boxer dogs. Vet Pathol. 2009 Jul; 46(4):684-7. [PubMed: 19276068]
  • Shaffer LG, Ramirez CJ, Sundin K, Carl C, Ballif BC (2015) Genetic screening and mutation identification in a rare canine breed, the Drentsche patrijshond. Vet Rec Case Rep. 3:e000185.
  • Shaffer LG, Ramirez CJ, Sundin K, Connell LB, Ballif BC (2016) Genetic screening and mutation identification in a rare canine breed, the Cesky fousek. Vet Rec Case Rep. 4:e000346.
  • Shelton GD, Johnson GC, O’Brien DP, Katz ML, Pesayco JP, Chang BJ, Mizisin AP, Coates JR. Degenerative myelopathy associated with a missense mutation in the superoxide dismutase 1 (SOD1) gene progresses to peripheral neuropathy in Pembroke Welsh Corgis and Boxers. J Neurol Sci. 2012 Jul 15;318(1-2):55-64. [PubMed: 22542607]
  • Zeng R, Coates JR, Johnson GC, Hansen L, Awano T, Kolicheski A, Ivansson E, Perloski M, Lindblad-Toh K, O'Brien DP, Guo J, Katz ML, Johnson GS. Breed Distribution of SOD1 Alleles Previously Associated with Canine Degenerative Myelopathy. J Vet Intern Med. 2014 Feb 13. doi: 10.1111/jvim.12317. [PubMed: 24524809]

Muscular Dystrophy (Golden Retriever Type)

 Other Names:Duchenne-type muscular dystrophy, Dystrophin muscular dystrophy, DMD, GRMD Genes:DMDInheritance:X-Linked RecessiveMutation:Point Mutation

Common Symptoms

Golden Retriever muscular dystrophy is an inherited disease affecting Golden Retrievers. Affected dogs are unable to produce adequate amounts of a protein important for muscle contraction and relaxation. By 10 weeks of age affected puppies are noticeably smaller than littermates shortly after birth due to decreased growth associated with the inability to nurse. Affected dogs often need to be hand or bottle fed to prevent starvation. Beginning around 6 weeks of age, dogs begin to develop a progressively abnormal gait, muscle weakness, excessive drooling, muscle Atrophy of the head and trunk, abnormal extension or flexion of joints and a “roach backed” appearance in the lumbar spine that eventually progresses to a concave flexion. Affected dogs may also suffer from aspiration pneumonia and cardiac disease. The prognosis is related to disease severity with some dogs dying soon after birth due to disease complications and others surviving for years with only mild symptoms.

Breed-Specific Information for the Golden Retriever

The Mutation of the DMD gene associated with Golden Retriever muscular dystrophy has been identified in Golden Retrievers, although its overall frequency in this breed is unknown.

Testing Tips

Genetic testing of the DMD gene in Golden Retrievers will reliably determine whether a dog is a genetic Carrierof Golden Retriever muscular dystrophy. Golden Retriever muscular dystrophy is inherited in an X-Linked Recessivemanner in dogs meaning that female dogs with one copy of the Mutation are carriers and that affected female dogs must receive two copies of the mutated gene (one from each parent) to develop the disease while male dogs only require one copy of the mutated gene from the mother in order to develop disease. Therefore, male dogs more commonly present with symptoms of the disease. Each male pup that is born to a female dog known to be a carrier of Golden Retriever muscular dystrophy has a 50% chance of inheriting the disease. Female dogs that are not carriers of this mutation have no increased risk of having affected pups. Reliable genetic testing is important for determining breeding practices. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers is not recommended. Golden Retrievers that are not carriers of the mutation have no increased risk of having affected pups.

There may be other causes of this condition in dogs and a normal result does not exclude a different mutation in this gene or any other gene that may result in a similar genetic disease or trait.

References

  • Brinkmeyer-Langford C, Kornegay JN. Comparative genomics of X-linked muscular dystrophies: The Golden Retriever Model. Curr Genomics. 2013 Aug;14(5):330-42. doi: 10.2174/13892029113149990004. [PubMed: 24403852]
  • Kornegay JN, Bogan JR, Bogan DJ, Childers MK, Li J, Nghiem P, Detwiler DA, Larsen CA, Grange RW, Bhavaraju-Sanka RK, Tou S, Keene BP, Howard JF, Jr., Wang J, Fan Z, Schatzberg SJ, Styner MA, Flanigan KM, Xiao X, Hoffman EP. Canine models of Duchenne muscular dystrophy and their use in therapeutic strategies. Mamm Genome. 2012 Feb;23(1-2):85-108. doi: 10.1007/s00335-011-9382-y. Epub 2012 Jan 5. Review. [PubMed: 22218699]
  • Sharp NJ, Kornegay JN, Van Camp SD, Herbstreith MH, Secore SL, Kettle S, Hung WY, Constantinou CD, Dykstra MJ, Roses AD, Bartlett RJ. An error in dystrophin mRNA processing in golden retriever muscular dystrophy, an animal homologue of Duchenne muscular dystrophy. Genomics. 1992 May;13(1):115-21. [PubMed: 1577476]

Dystrophic Epidermolysis Bullosa-Results-Clear

 Other Names:Recessive dystrophic epidermolysis bullosa, DEB, EB, RDEBAffected Genes:COL7A1Inheritance:Autosomal RecessiveMutation:Point Mutation

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Common Symptoms

Dystrophic Epidermolysis Bullosa (DEB) is a hereditary skin disease affecting Golden Retrievers. Clinical signs of DEB are present at birth. Affected dogs have fragile skin that is easily damaged from rubbing or trauma resulting in blisters, ulcers and scarring of the skin. Areas that are most prone to blisters are the face, foot pads, genital areas and ears. In addition, affected dogs will develop blisters and ulcers inside the mouth and in the esophagus. Ulcerations of the skin and mucous membranes are painful and can become infected. Blistering of the skin tends to cease at around 8 months of age however, ulcers of the mouth and esophagus persist into adulthood. Dogs with DEB are often smaller than littermates, likely due to difficulties eating.

Breed-Specific Information for the Golden Retriever

The Mutation of the COL7A1 gene associated with dystrophic epidermolysis bullosa has been identified in Golden Retrievers, although its overall frequency in this breed is unknown.

Testing Tips

Genetic testing of the COL7A1 gene in Golden Retrievers will reliably determine whether a dog is a genetic Carrier of dystrophic epidermolysis bullosa. Dystrophic Epidermolysis Bullosa is inherited in an Autosomal Recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. In general, carrier dogs do not have features of the disease but when bred with another carrier of the same Mutation, there is a risk of having affected pups. Each pup that is born to this pairing has a 25% chance of inheriting the disease and a 50% chance of inheriting one copy and being a carrier of the COL7A1 gene mutation. Reliable genetic testing is important for determining breeding practices. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers to each other is not recommended. Golden Retrievers that are not carriers of the mutation have no increased risk of having affected pups.

There may be other causes of this condition in dogs and a normal result does not exclude a different mutation in this gene or any other gene that may result in a similar genetic disease or trait.

References

  • Baldeschi C, Gache Y, Rattenholl A, Bouillé P, Danos O, Ortonne JP, Bruckner-Tuderman L, Meneguzzi G. Genetic correction of canine dystrophic epidermolysis bullosa mediated by retroviral vectors. Hum Mol Genet. 2003 Aug 1; 12(15):1897-905. [PubMed: 12874109]
  • Gache Y, Pin D, Gagnoux-Palacios L, Carozzo C, Meneguzzi G. Correction of dog dystrophic epidermolysis bullosa by transplantation of genetically modified epidermal autografts. J Invest Dermatol. 2011 Oct; 131(10):2069-78.[PubMed: 21697889]
  • Palazzi X, Marchal T, Chabanne L, Spadafora A, Magnol JP, Meneguzzi G. Inherited dystrophic epidermolysis bullosa in inbred dogs: A spontaneous animal model for somatic gene therapy. J Invest Dermatol. 2000 Jul; 115(1):135-7. [PubMed: 10886525]

Osteogenesis Imperfecta (Golden Retriever Type)

 Other Names:Brittle bone disease, OI

Genes:COL1A1Inheritance:Autosomal DominantMutation:Point Mutation


Common Symptoms

Osteogenesis imperfecta (OI) is an inherited Collagen disorder affecting dogs. Affected dogs typically present between 3 to 4 weeks of age with pain, lameness and fractures. OI is caused by a defect is in the way collagen is made. Because collagen is an important component of bone, bones of affected dogs are thinner than normal, fracture easily and do not heal properly. Other features of the disorder include loose joints and brittle teeth. Affected puppies may die shortly after birth and be smaller than littermates. Because of the severity of the disease, pups with OI are usually euthanized by 3 months of age.

Breed-Specific Information for the Golden Retriever

The Mutation in the COL1A1 gene associated with osteogenesis imperfecta (golden retriever type) has been identified in a golden retriever, although its overall frequency in this breed is unknown.

Testing Tips

Genetic testing of the COL1A2 gene will reliably determine whether a dog is a genetic Carrier of osteogenesis imperfecta (golden retriever type). Osteogenesis imperfecta (golden retriever type) is inherited in an Autosomal Dominant manner in dogs meaning that they only need to inherit one copy of the mutated gene to develop the disease. Each pup that is born to a parent carrying one copy of the Mutation has a 50% chance of inheriting one copy of the COL1A2 gene mutation and developing the disease. Reliable genetic testing is important for determining breeding practices. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers is not recommended. Dogs that are not carriers of the mutation have no increased risk of having affected pups.

There may be other causes of this condition in dogs and a normal result does not exclude a different mutation in this gene or any other gene that may result in a similar genetic disease or trait.

References

  • Campbell BG, Wootton JA, MacLeod JN, Minor RR. Sequence of normal canine COL1A1 cDNA and identification of a heterozygous alpha1(I) collagen Gly208Ala mutation in a severe case of canine osteogenesis imperfecta. Arch Biochem Biophys. 2000 Dec 1; 384(1):37-46. [PubMed: 11147834]

Sensory Ataxic Neuropathy

 Other Names:SAN Genes:tRNA-TyrInheritance:MitochondrialMutation:Deletion

Common Symptoms

Sensory Ataxic Neuropathy is an inherited neurologic condition affecting Golden Retrievers. Affected dogs typically present between 2 to 8 months of age with signs of neurologic disease. Symptoms include a lack of muscle coordination, abnormal gait and difficulty balancing especially affecting the hind limbs. Muscle mass appears normal and the condition does not appear to be painful. Although the disease progresses slowly, dogs are often humanely euthanized before three years of age.

Breed-Specific Information for the Golden Retriever

The Mutation of the tRNA-Tyr gene associated with sensory ataxic neuropathy has been identified in Golden Retrievers, although its overall frequency in this breed is unknown.

Testing Tips

Genetic testing of the tRNA-Tyr gene will reliably determine whether a dog is a genetic Carrier of sensory ataxic neuropathy. Sensory Ataxic Neuropathy is a mitochondrial disorder. Dogs only inherit mitochondrial DNA from the mother. Because this disease is inherited in a maternal inheritance pattern, both male and female dogs must inherit the mutated gene from the mother to develop the disease. Affected male dogs do not pass their mitochondrial DNA to their offspring and cannot produce affected pups. Each pup that is born to a female dog carrying a Mutation in the tRNA-Tyr gene is at risk of having the disease. However, the ratio of mitochondria without the mutation to the number of mitochondria with the mutation is important in determining whether a specific dog will actually develop features of the disease. Reliable genetic testing is important for determining breeding practices. Because disease presentation is variable, genetic testing should be performed before breeding. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of carrier or affected female dogs is not recommended. Dogs that are not carriers of the mutation have no increased risk of having affected pups.

There may be other causes of this condition in dogs and a normal result does not exclude a different mutation in this gene or any other gene that may result in a similar genetic disease or trait.

References

  • Baranowska I, Jäderlund KH, Nennesmo I, Holmqvist E, Heidrich N, Larsson NG, Andersson G, Wagner EG, Hedhammar A, Wibom R, Andersson L. Sensory ataxic neuropathy in golden retriever dogs is caused by a deletion in the mitochondrial tRNATyr gene. PLoS Genet. 2009 May; 5(5):e1000499. [PubMed: 19492087]
  • Jäderlund KH, Orvind E, Johnsson E, Matiasek K, Hahn CN, Malm S, Hedhammar A. A neurologic syndrome in Golden Retrievers presenting as a sensory ataxic neuropathy. J Vet Intern Med. 2007 Nov-Dec; 21(6):1307-15.[PubMed: 18196741]