Health Testing's One on One
Our whole purpose or mission per say is to promote the health and welfare of companion stndard poodles, through a reduction in the incidence of all genetic diseases. We strive to buy from health tested lines and to improve our lines as we breed by continuing our own health testing on our poodles we breed., We try to research our lines to make sure they are the best possible match using low coi's and genetic issues like vwd, dm, ne etc. By all means we can not totally make our lines perfect but we strive to lower the chances of any hereditary genetic issues.
Below I give you all the genetic testing we do on our breeding Poodles and the meaning of those tests. Poodles carry these genetic traits that could affect the life of your new puppy.
DM
DM stands for Degenerative Myelopathy or (DM) for short.
This is a progressive neurological disorder that affects the spinal cord of dogs. Dogs that have inherited two defective copies will experience a breakdown of the cells responsible for sending and receiving signals from the brain, resulting in neurological symptoms.
This disease often begins with an unsteady gait, and the dog may wobble when they attempt to walk. As the disease progresses, the dog's hind legs will weaken and eventually the dog will be unable to walk at all. Degenerative Myelopathy moves up the body, so if the disease is allowed to progress, the dog will eventually be unable to hold his bladder and will lose normal function in its front legs. Fortunately, there is no direct pain associated with Degenerative Myelopathy.
The onset of Degenerative Myelopathy generally occurs later in life starting at an average age of about 8 years. However, some dogs may begin experiencing symptoms much earlier, some later, and a small percentage of dogs that have inherited two copies of the mutation will not experience symptoms at all. Thus, this disease is not completely penetrant, meaning that while a dog with the mutation is highly likely to develop Degenerative Myelopathy, the disease does not affect every dog that has the genotype....
NEwS
NEwS STANDS FOR Neonatal Encephalopathy with Seizures OR (NEwS) FOR SHORT;
This is an autosomal recessive disease of standard poodle puppies. Affected puppies are small and weak at birth. Many die in their first week of life. Those surviving past 1 week develop ataxia, a whole-body tremor and by 4 to 6 weeks of age, severe generalized clonic-tonic seizures. None have survived to 7 weeks of age. Cerebella from affected puppies were reduced in size.
This fatal disease affects the brain of newborn puppies causing weakness and seizures and ultimately death within a few weeks of birth. Neonatal encephalopathy is recessive — both parents must possess the gene mutation in order to produce offspring affected by the disease. Dogs with one copy of this gene do not show symptom, but are carriers and can pass the gene to their offspring.
vWD1
vWD1 STANDS FOR von Willebrand's Disease Type I OR vWD FOR SHORT;
This is an inherited bleeding disorder that inhibits the normal blood clotting process, causing prolonged bleeding after an injury. People with this condition often experience excessive bruising, prolonged nosebleeds, and excessive bleeding following any form of trauma, including surgery, or dental work.
The primary function of von Willebrand factor (vWF) a blood glycoprotein, is to bind itself to other proteins. The deficiency or failure of vWF function inhibits the blood coagulation process and causes bleeding which is most apparent in tissues having high blood flow or narrow vessels.
Von Willebrand's disease type I (vWDI): In dogs (as well as in people), three separate types of vWD have been identified. Of these three types there are five different genetic mutations causing vWDs in dogs. Genetic tests have been developed to identify all five variants. Von Willebrand's disease type I (VWDI) is transmitted as an autosomal recessive trait with variable penetrance and is the least serious of the three.
Pra
The OptiGen prcd-PRA test is a DNA-based test that helps you avoid one form of Progressive Retinal Atrophy (PRA). PRA refers to a group of diseases that cause the retina of the eye to degenerate slowly over time. The result is declining vision and eventual blindness.
OFA
OFA OR ORTHOPEDIC FOUNDATION FOR ANIMALS; This is the big form of what is known as Hip Dysplasia... we have our breeding dogs checked by our vet for good hips, and every other generation we send in to OFA.
WHAT IS HIP DYSPLASIA?
Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.
The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged.
With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.
AN EXAMINATION OF HIP GRADING;
The phenotypic evaluation of hips done by the Orthopedic Foundation for Animals falls into seven different categories. Those categories are Normal (Excellent, Good, fair), Borderline, and Dysplastic (Mild, Moderate, Severe). Once each of the radiologists classifies the hip into one of the 7 phenotypes above, the final hip grade is decided by a consensus of the 3 independent outside evaluations. Examples would be:
Our whole purpose or mission per say is to promote the health and welfare of companion stndard poodles, through a reduction in the incidence of all genetic diseases. We strive to buy from health tested lines and to improve our lines as we breed by continuing our own health testing on our poodles we breed., We try to research our lines to make sure they are the best possible match using low coi's and genetic issues like vwd, dm, ne etc. By all means we can not totally make our lines perfect but we strive to lower the chances of any hereditary genetic issues.
Below I give you all the genetic testing we do on our breeding Poodles and the meaning of those tests. Poodles carry these genetic traits that could affect the life of your new puppy.
DM
DM stands for Degenerative Myelopathy or (DM) for short.
This is a progressive neurological disorder that affects the spinal cord of dogs. Dogs that have inherited two defective copies will experience a breakdown of the cells responsible for sending and receiving signals from the brain, resulting in neurological symptoms.
This disease often begins with an unsteady gait, and the dog may wobble when they attempt to walk. As the disease progresses, the dog's hind legs will weaken and eventually the dog will be unable to walk at all. Degenerative Myelopathy moves up the body, so if the disease is allowed to progress, the dog will eventually be unable to hold his bladder and will lose normal function in its front legs. Fortunately, there is no direct pain associated with Degenerative Myelopathy.
The onset of Degenerative Myelopathy generally occurs later in life starting at an average age of about 8 years. However, some dogs may begin experiencing symptoms much earlier, some later, and a small percentage of dogs that have inherited two copies of the mutation will not experience symptoms at all. Thus, this disease is not completely penetrant, meaning that while a dog with the mutation is highly likely to develop Degenerative Myelopathy, the disease does not affect every dog that has the genotype....
NEwS
NEwS STANDS FOR Neonatal Encephalopathy with Seizures OR (NEwS) FOR SHORT;
This is an autosomal recessive disease of standard poodle puppies. Affected puppies are small and weak at birth. Many die in their first week of life. Those surviving past 1 week develop ataxia, a whole-body tremor and by 4 to 6 weeks of age, severe generalized clonic-tonic seizures. None have survived to 7 weeks of age. Cerebella from affected puppies were reduced in size.
This fatal disease affects the brain of newborn puppies causing weakness and seizures and ultimately death within a few weeks of birth. Neonatal encephalopathy is recessive — both parents must possess the gene mutation in order to produce offspring affected by the disease. Dogs with one copy of this gene do not show symptom, but are carriers and can pass the gene to their offspring.
vWD1
vWD1 STANDS FOR von Willebrand's Disease Type I OR vWD FOR SHORT;
This is an inherited bleeding disorder that inhibits the normal blood clotting process, causing prolonged bleeding after an injury. People with this condition often experience excessive bruising, prolonged nosebleeds, and excessive bleeding following any form of trauma, including surgery, or dental work.
The primary function of von Willebrand factor (vWF) a blood glycoprotein, is to bind itself to other proteins. The deficiency or failure of vWF function inhibits the blood coagulation process and causes bleeding which is most apparent in tissues having high blood flow or narrow vessels.
Von Willebrand's disease type I (vWDI): In dogs (as well as in people), three separate types of vWD have been identified. Of these three types there are five different genetic mutations causing vWDs in dogs. Genetic tests have been developed to identify all five variants. Von Willebrand's disease type I (VWDI) is transmitted as an autosomal recessive trait with variable penetrance and is the least serious of the three.
Pra
The OptiGen prcd-PRA test is a DNA-based test that helps you avoid one form of Progressive Retinal Atrophy (PRA). PRA refers to a group of diseases that cause the retina of the eye to degenerate slowly over time. The result is declining vision and eventual blindness.
OFA
OFA OR ORTHOPEDIC FOUNDATION FOR ANIMALS; This is the big form of what is known as Hip Dysplasia... we have our breeding dogs checked by our vet for good hips, and every other generation we send in to OFA.
WHAT IS HIP DYSPLASIA?
Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.
The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged.
With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.
AN EXAMINATION OF HIP GRADING;
The phenotypic evaluation of hips done by the Orthopedic Foundation for Animals falls into seven different categories. Those categories are Normal (Excellent, Good, fair), Borderline, and Dysplastic (Mild, Moderate, Severe). Once each of the radiologists classifies the hip into one of the 7 phenotypes above, the final hip grade is decided by a consensus of the 3 independent outside evaluations. Examples would be:
- Two radiologists reported Excellent, one Good—the final grade would be Excellent.
- One radiologist reported Excellent, one Good, one Fair—the final grade would be Good.
- One radiologist reported Fair, two radiologists reported Mild—the final grade would be Mild.
REMEMBER NORMAL = EXCELLENT, GOOD, AND FAIR SHOWN BELOW;

Excellent:
This classification is assigned for superior conformation in comparison to other animals of the same age and breed. There is a deep seated ball (femoral head) which fits tightly into a well-formed socket (acetabulum) with minimal joint space. There is almost complete coverage of the socket over the ball.

Good:
This classification is assigned for slightly less than superior but a well-formed congruent hip joint is visualized. The ball fits well into the socket and good coverage is present.

Fair:
This classification is assigned for minor irregularities in the hip joint exist. The hip joint is wider than a good hip phenotype. This is due to the ball slightly slipping out of the socket causing a minor degree of joint incongruency. There may also be slight inward deviation of the weight-bearing surface of the socket (dorsal acetabular rim) causing the socket to appear slightly shallow. This can be a normal finding in some breeds however, such as the Chinese Shar Pei, Chow Chow, and Poodle.
Borderline:
Is no clear cut consensus between the radiologists to place the hip into a given category of normal or dysplastic. There is usually more incongruency present than what occurs in the minor amount found in a fair but there are no arthritic changes present that definitively diagnose the hip joint being dysplastic. There also may be a bony projection present on any of the areas of the hip anatomy illustrated above that can not accurately be assessed as being an abnormal arthritic change or as a normal anatomic variant for that individual dog. To increase the accuracy of a correct diagnosis, it is recommended to repeat the radiographs at a later date (usually 6 months). This allows the radiologist to compare the initial film with the most recent film over a given time period and assess for progressive arthritic changes that would be expected if the dog was truly dysplastic. Most dogs with this grade (over 50%) show no change in hip conformation over time and receive a normal hip rating; usually a fair hip phenotype.
REMEMBER BORDERLINE AND DYSPLASTIC = BORDERLINE RATINGS;

Mild
This classification is assigned for Hip Dysplasia: there is significant subluxation present where the ball is partially out of the socket causing an incongruent increased joint space. The socket is usually shallow only partially covering the ball. There are usually no arthritic changes present with this classification and if the dog is young (24 to 30 months of age), there is an option to resubmit an radiograph when the dog is older so it can be reevaluated a second time. Most dogs will remain dysplastic showing progression of the disease with early arthritic changes. Since HD is a chronic, progressive disease, the older the dog, the more accurate the diagnosis of HD (or lack of HD).
This classification is assigned for Hip Dysplasia: there is significant subluxation present where the ball is partially out of the socket causing an incongruent increased joint space. The socket is usually shallow only partially covering the ball. There are usually no arthritic changes present with this classification and if the dog is young (24 to 30 months of age), there is an option to resubmit an radiograph when the dog is older so it can be reevaluated a second time. Most dogs will remain dysplastic showing progression of the disease with early arthritic changes. Since HD is a chronic, progressive disease, the older the dog, the more accurate the diagnosis of HD (or lack of HD).

Moderate
This classification is assigned when there is significant subluxation present where the ball is barely seated into a shallow socket causing joint incongruency. There are secondary arthritic bone changes usually along the femoral neck and head (termed remodeling), acetabular rim changes (termed osteophytes or bone spurs) and various degrees of trabecular bone pattern changes called sclerosis. Once arthritis is reported, there is only continued progression of arthritis over time.
This classification is assigned when there is significant subluxation present where the ball is barely seated into a shallow socket causing joint incongruency. There are secondary arthritic bone changes usually along the femoral neck and head (termed remodeling), acetabular rim changes (termed osteophytes or bone spurs) and various degrees of trabecular bone pattern changes called sclerosis. Once arthritis is reported, there is only continued progression of arthritis over time.

Severe;
This classification is assigned when there are radiographic evidence of marked dysplasia exists. There is significant subluxation present where the ball is partly or completely out of a shallow socket. Like moderate HD, there are also large amounts of secondary arthritic bone changes along the femoral neck and head, acetabular rim changes and large amounts of abnormal bone pattern changes.
This classification is assigned when there are radiographic evidence of marked dysplasia exists. There is significant subluxation present where the ball is partly or completely out of a shallow socket. Like moderate HD, there are also large amounts of secondary arthritic bone changes along the femoral neck and head, acetabular rim changes and large amounts of abnormal bone pattern changes.
Some very important hip information I have listed below;
Four major influences of getting hip dysplasia in your four legged companion continues with some results that may surprise you.
1-GENETIC CAUSES
2-POOR DIET
3-OVER FEEDING
4-TOO MUCH EXERCISE AT A YOUNG AGE
By all of the research these conclusions even surprised me.
Research has found that genetics play only between 25% and 30% role in a dog having or getting hip dysplasia. This is according to a study done by the German Shepherd dog club of Germany.
So what does this mean to you as a dog owner ? Welll this means that new owners can assume a great deal of responsibility (70% - 75%) in their dogs developing good hips.
What is it you can do to prevent this from happening ?
Below is what you as an owner can do to help drastically in preventing bad hips in your new puppies advancement to adulthood:
1- Keeping your dog on the thin side, be able to see a definition between the ribs and the loins of your dog. The more weight a dog carries the more pressure is on the hips. This is extremely important when the dog is growing starting at eight weeks of age, too much weight at a young age is going to add stress on soft puppy bones.
2- Do not over exercise your young dog/puppy like jogging/running with your puppy. Pulling weights, pulling with owner on a bike etc. will cause problems as well, Allowing your puppy to jump from a vehicle etc. Do not take your puppy jogging, at least until it's older than a year of yage. overly exercised is the fastest way to destroy a puppies hips. Do not exercise to the point of exhaustion or take the pup for long long walks. a walk around the block is fine but a two mile walk is not fine.
3- Feed a quality puppy food. Feeding a controlled balanced diet increases the opportunity for muscle connective tissue and the hip joint bones to develop congruently.
4- Taking your dog/puppy for a swim, can help exercise your dog or puppy without hurting them., it is way better than jogging.
One of the most common myths about hip dysplasia is that it is equal to a death sentence or a life of crippling pain for your dog, this is rarely the case.
So proper exercise and good nutrition is priority in healthy bones.
COI
COI IS NOT A GENETIC TEST BUT A PERCENTAGE USED TO HELP BREEDERS KEEP GENERATIONS APART IN THEIR LINES, THIS IS ALSO TO LOWER THE RISK OF PASSING ON GENETIC ABNORMALITIES IN OUR DOGS AND THEIR LINES.... A DOGS PEDIGREE IS BEING RESEARCHED IN THIS CASE TO VERIFY A RESULT ON HOW MUCH INBREEDING HAS BEEN TAKING PLACE FOR MANY GENERATIONS. MOST VETS BELIEVE THAT YOU SHOULD STRIVE FOR A COI ON A DOG TO BE KEPT UNDER 6% AS A NORM. BREEDERS KEEPING TRACK OF THIS IN THEIR LINES WILL DRAMATICALLY REDUCE THE RISK OF GENETIC HEALTH ISSUES AND KEEPING THEIR GENE POOL CLEAN... A GOOD BREEDER WILL LEAVE THREE GENERATIONS APART FROM A BREEDING PAIR OF DOGS
Four major influences of getting hip dysplasia in your four legged companion continues with some results that may surprise you.
1-GENETIC CAUSES
2-POOR DIET
3-OVER FEEDING
4-TOO MUCH EXERCISE AT A YOUNG AGE
By all of the research these conclusions even surprised me.
Research has found that genetics play only between 25% and 30% role in a dog having or getting hip dysplasia. This is according to a study done by the German Shepherd dog club of Germany.
So what does this mean to you as a dog owner ? Welll this means that new owners can assume a great deal of responsibility (70% - 75%) in their dogs developing good hips.
What is it you can do to prevent this from happening ?
Below is what you as an owner can do to help drastically in preventing bad hips in your new puppies advancement to adulthood:
1- Keeping your dog on the thin side, be able to see a definition between the ribs and the loins of your dog. The more weight a dog carries the more pressure is on the hips. This is extremely important when the dog is growing starting at eight weeks of age, too much weight at a young age is going to add stress on soft puppy bones.
2- Do not over exercise your young dog/puppy like jogging/running with your puppy. Pulling weights, pulling with owner on a bike etc. will cause problems as well, Allowing your puppy to jump from a vehicle etc. Do not take your puppy jogging, at least until it's older than a year of yage. overly exercised is the fastest way to destroy a puppies hips. Do not exercise to the point of exhaustion or take the pup for long long walks. a walk around the block is fine but a two mile walk is not fine.
3- Feed a quality puppy food. Feeding a controlled balanced diet increases the opportunity for muscle connective tissue and the hip joint bones to develop congruently.
4- Taking your dog/puppy for a swim, can help exercise your dog or puppy without hurting them., it is way better than jogging.
One of the most common myths about hip dysplasia is that it is equal to a death sentence or a life of crippling pain for your dog, this is rarely the case.
So proper exercise and good nutrition is priority in healthy bones.
COI
COI IS NOT A GENETIC TEST BUT A PERCENTAGE USED TO HELP BREEDERS KEEP GENERATIONS APART IN THEIR LINES, THIS IS ALSO TO LOWER THE RISK OF PASSING ON GENETIC ABNORMALITIES IN OUR DOGS AND THEIR LINES.... A DOGS PEDIGREE IS BEING RESEARCHED IN THIS CASE TO VERIFY A RESULT ON HOW MUCH INBREEDING HAS BEEN TAKING PLACE FOR MANY GENERATIONS. MOST VETS BELIEVE THAT YOU SHOULD STRIVE FOR A COI ON A DOG TO BE KEPT UNDER 6% AS A NORM. BREEDERS KEEPING TRACK OF THIS IN THEIR LINES WILL DRAMATICALLY REDUCE THE RISK OF GENETIC HEALTH ISSUES AND KEEPING THEIR GENE POOL CLEAN... A GOOD BREEDER WILL LEAVE THREE GENERATIONS APART FROM A BREEDING PAIR OF DOGS