​​​Gems Standard Poodles


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Health Testing

Most breeders will try and eliminate these diseases from their lines...something to look for in the 
breeder as well to see what kind of testings has been done to the parents of a potential puppy.

Degenerative Myelopathy (DM)

This is a progressive disease of the spinal cord in older dogs. Onset is usually between 7 and 14 years, 
and usually begins with a loss of coordination in the hind limbs.

Certified Eye Registration Foundation (CERF)

This is dedicated to the elimination of heritable eye disease in purebred dogs through registration and 
research. The organization was founded by a group of concerned, purebred owners/breeders who 
recognized that the quality of their dogs' lives were being affected by heritable eye disease. CERF was 
then established in conjunction with cooperating, board certified, veterinary ophthalmologists, as a 
means to accomplish the goal of elimination of heritable eye disease in all purebred dogs by forming a 
centralized, national registry.

Neonatal Encephalopathy (NE)

This is a fatal disease of the brain in newborn Standard Poodles. Affected pups are weak, 
uncoordinated, and mentally dull from birth. If they survive the first few days, their growth may be 
stunted. When normal puppies in the litter start walking, some pups with NE cannot stand at all and 
others struggle to their feet with jerky steps, falling frequently. Seizures develop in most at 4-5 weeks, 
and the puppies die or are euthanized before they reach weaning age.


von Willebrand Disease (vWD)

This is the most commonly inherited bleeding disorder in dogs and has been reported in over 50 
breeds, but it is most prevalent in the Corgi, Doberman Pinscher, German Shepherd Dog, German 
Shorthaired Pointer, Golden Retriever, Shetland Sheepdog and Standard Poodle. It is caused by a 
deficiency in the amount of a certain protein called von Willebrand factor, or vWF. vWF’s main 
function is to transport and bind coagulation factor VIII to injured blood vessels. The ‘type’ of vWD is 
partly determined by the amount of vWF in the blood.

vWD Type I

Is the most mild form and has been observed in the most breeds. Dogs with this type still produce vWF 
at varying degrees. Some possess enough that they may never be diagnosed, while others produce so 
little that they may suffer disproportionate bleeding following: injury, spaying/ neutering, ear 
cropping, tail docking.

vWD Type II

Is a very rare form found primarily in the German Shorthaired and German Wirehaired Pointers. 
Dogs with this type still produce vWF, but there are structural abnormalities that affect its function, 
and lead to more severe bleeding episodes.

vWD Type III

Is the most severe form of vWD, and is found primarily in the Shetland Sheepdog and Scottish Terrier. 
Dogs with this type produce virtually no vWF, and will usually have several bleeding episodes before 
reaching adulthood.


Sebaceous Adenitis (SA)

This is a hereditary skin disease in which the sebaceous glands become inflamed, often leading to 
progressive loss of hair. The disease is primarily seen in Standard Poodles, Akitas, and Samoyeds, 
although there have been reported cases in a number of other breeds and mixed breeds as well. The 
disease can develop in a wide age range, with age of onset documented as early as 1 year and as late 
as 12 years. Males and females appear to be affected equally. The exact mode of inheritance is 
unknown. SA can be difficult as the symptoms vary by breed, the symptoms are similar to those of 
other diseases such as hypothyroidism or allergies, and the disease can vary greatly in its severity. 
Visible symptoms include excessive dandruff or scaling, hair loss, lesions, a musty odor, and even 
secondary skin infections. On the other hand, dogs affected with SA can be subclinical and show no 
outward signs of the disease. There is no DNA test available to genotypically detect SA. Currently, 
diagnosis is based on skin biopsy samples, and unfortunately the current screening method may result 
in false negatives. Because the age of onset varies, and since this is only a phenotypic test reflecting a 
point in time, retesting is recommended every 1 to 2 years for dogs used in breeding programs.

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.

ELBOW DYSPLASIA TYPES
THE THREE FACES OF ELBOW DYSPLASIA
ELBOW DYSPLASIA IS A GENERAL TERM USED TO IDENTIFY AN INHERITED POLYGENIC 
DISEASE IN THE ELBOW OF DOGS. THREE SPECIFIC ETIOLOGIES MAKE UP THIS DISEASE AND 
THEY CAN OCCUR INDEPENDENTLY OR IN CONJUNCTION WITH ONE ANOTHER. THESE 
ETIOLOGIES INCLUDE:
Pathology involving the medial coronoid of the ulna (FCP)
Osteochondritis of the medial humeral condyle in the elbow joint (OCD)
Ununited anconeal process (UAP)
Studies have shown the inherited polygenic traits causing these etiologies are independent of one 
another. Clinical signs involve lameness which may remain subtle for long periods of time. No one can 
predict at what age lameness will occur in a dog due to a large number of genetic and environmental 
factors such as degree of severity of changes, rate of weight gain, amount of exercise, etc. Subtle 
changes in gait may be characterized by excessive inward deviation of the paw which raises the 
outside of the paw so that it receives less weight and distributes more mechanical weight on the 
outside (lateral) aspect of the elbow joint away from the lesions located on the inside of the joint. 
Range of motion in the elbow is also decreased.


Cushings

There are 3 forms of Cushings Disease. Most dogs have the more common form, Pituitary Dependent 
PD. With this form the dogs have a slow growing form of cancer that is located in the pituitary gland. 
This causes the adrenal glands to produce too much cortisol because the tumor triggers too much 
ACTH to be produced. The next form is the Non Pituitary. Here there is a tumor in one or both of the 
adrenal glands. Here also too much cortisol is produced as a result of the tumor. The tumor is often 
malignant and is called an Adenocarcinoma. It is aggressive and it can spread to other parts of the 
body and organs. The non-cancerous tumor is called Adenoma. The last form comes from dogs being 
on long term use of "Cortisone". This drug comes in many forms and can cause problems with its long 
term use. This long term usage makes the body think it has more cortisone than it really does leading 
the body to misread the actual amount it has. There are many warning signs of Cushings. Some of the 
more common ones are: excessive appetite, drinking large amounts of water, frequent urination, large 
pot belly, thin skin, hair loss on the body, thinning of hair and drastic change of texture of hair. This 
is usually seen in older dogs, but can begin much earlier in life. It can be very slow in progressing. 
There are tests to tell you if your dog has Cushings. If you suspect it, call your vet and get proper 
testing done to get a correct diagnosis.


Patellar Luxation

Patellar luxation is the dislocation (slipping) of the patella (kneecap). In dogs the patella is a small 
bone that shields the front of the stifle joint. This bone is held in place by ligaments. As the knee joint 
is moved, the patella slides in a grove in the femur. The kneecap may dislocate toward the inside 
(medial) or outside (lateral) of the leg. This condition may be the result of injury or congenital 
deformities (present at birth). Patellar luxation can affect either or both legs. The most common 
occurrence of luxating patella is the medial presentation in small or miniature dog breeds. Shallow 
femoral groove, weak ligaments and malalignment of the tendons and muscles that straighten the 
joint are all conditions that will predispose a dog toward luxating patellae.
Indications of patellar luxation are; difficulty in straightening the knee, pain in the stifle, limping, or 
the tip of the hock points outward while the toes point inward.


Grade 1:
Intermittent patellar luxation - occasional carrying of the affected limb. The patella can easily be 
manually luxated at full extension of the stifle, but returns to proper position when pressure is released.


Grade 2:
Frequent patellar luxation - in some cases luxation is more or less permanent. The affected limb is 
sometimes carried, although the dog may walk with the stifle slightly flexed.


Grade 3: Permanent patellar luxation - even though the patella is luxated, many animals will walk 
with the limb in a semi-flexed position.

Grade 4: Permanent patellar luxation - the affected limb is either carried or the animal walks in a 
crouched position, with the limb partially flexed.

Some important hip information is stated below:

HIP DYSPLASIA HAS FOUR MAJOR CAUSES:<p> </p>1-GENETIC CAUSES

2-POOR DIET

3-OVER FEEDING

4-TOO MUCH EXERCISE AT A YOUNG AGE

Research has found that genetics play between a 25% and 30% role in a dog having hip dysplasia 
according to a study done by the German Shepherd Dog Club of Germany. This means that new 
owners can assume a great deal of responsibility (70% to 75%) in their dog developing good hips.




What you can do as the owner to help prevent bad hips in your puppy’s advancement to adulthood;

1- Keep your dog on the thin side– be able to see a definition between the ribs and 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 (between 8 weeks and 18 months) too much weight at a young age is going to add 
stress on soft puppy bones.

2- Do not over exercise your young dog. Over exercise (jogging/running with a puppy, pulling weights, 
running with owner on a bike etc.) will cause problems, as well as allowing it to jump from SUV's or 
trucks etc.  DO NOT TAKE A PUPPY JOGGING!!  Not until it's older than one year of age.  Over 
exercise is the fastest way to destroy puppy’s hips.   Do not exercise to the point of exhaustion, or take 
the pup for long long walks. A walk round the block is fine; a 2 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- Take your dog for a SWIM!! When your puppy reaches adulthood take the dog swimming every 
day for 3 or 4 months before you have x-rays taken. Swimming is the best exercise you can do for a 
dog.

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 the dog.  This is rarely the case.  

OFA classifies poor hips in categories of mild, moderate and severe.  Most dogs with Mild ratings and 
a good percentage of those diagnosed with Moderate ratings, lead perfectly normal, active, healthy 
lives with few, if any symptoms.  Many dogs even with ratings of mild or moderate are used as agility 
dogs, working dogs for the law enforcement and as search dogs.  They likely will develop some 
arthritis in the joints as they age, but then most dogs even with ratings of fair, good and excellent will 
suffer from some form of arthritis in their later years.  

Proper exercise and nutrition, along with joint supplements such as Nuvet Joint, glucosamine, 
chondroitin and vitamins can help slow the development of arthritis.  According to Dog Health Report 
“A lot of pain may be caused, in cases of hip dysplasia, to the dog due to the malformation of the hip 
joint and femur bones and in the some cases, will need immediate surgery, or in the worst case, will 
need to be put to sleep. Mild cases are easier to deal with, they mainly need a good diet and exercise 
routine.