River is now retired 

Here is a description of Rivers
I am listing this as an education, we want to be right up front so when you hear a breeder say 4 panel clear this is what it should look like.  Each of the panels tested is a description of what she was tested for this is standard testing for all French Bulldog Breeders. 

When reading the above certificates above in a nutshell of what its saying-

-Preliminary good hips

-2.4" trachea

-Normal cardiac

-Eyes normal

-Normal patella's

-Clear of HUU DM CMR1 JHC -Cystinuria variant, two and three

​

OFA Testing- 

​

Canine Hip Dysplasia 
https://ofa.org/diseases/hip-dysplasia/

 

Patellar Luxation
https://ofa.org/diseases/patellar-luxation/

 

Animal Eye (CAER)
https://ofa.org/diseases/eye-disease/

 

Congenital Cardiac Disease
https://ofa.org/diseases/cardiac-disease/

------------------------------------------
Canine Multifocal Retinopathy Type 1 and Type 2 (CMR1 and CMR2)

Description:
Canine Multifocal Retinopathy Type 1 and 2 (CMR1 and CMR2) is an autosomal recessive eye disorder known to affect Great Pyrenees, English Mastiffs, Bullmastiffs, Australian Shepherds, Dogue de Bordeaux, English Bulldogs, American Bulldogs, Coton de Tulears, Perro de Presa Canario, and Cane Corsos.

The mutation causes raised lesions to form on the retina. The lesions alter the appearance of the eye but usually do not affect sight. The lesions may disappear or may result in minor retinal folding. Symptoms of the mutation usually appear when a puppy is only a few months old, and generally do not worsen over time.

​

CMR is a recessive disorder. This means that a dog must inherit two copies of the mutation in order to exhibit symptoms of CMR. A dog with one copy of the mutation is known as a carrier. If two carriers are bred to one another, there is a 25% chance per puppy born that they will develop symptoms of CMR and a 50% chance per puppy born that they will also be carriers. Therefore, it is useful to test for the presence of the CMR mutation before breeding. Additionally, since retinal defects can be caused by other conditions, testing can verify that a dog actually has CMR rather than some other eye condition.

​

Results:
Animal Genetics offers DNA testing for Canine Multifocal Retinopathy Types 1. The genetic test verifies the presence of the recessive mutation and presents results as one of the following:

CMR/CMR    / Affected/  The dog carries two copies of the mutant gene and is homozygous for CMR. This dog will be affected and will always pass on a copy of the mutated gene to its offspring.

CMR/n / Carrier/  Both the normal and mutant copies of the gene detected. Dog is a carrier for the CMR mutation and can pass on a copy of the defective gene to its offspring 50% of the time.

​

River,  >  n/n  > Clear > Dog tested negative for the gene mutation that causes CMR and will not pass on the defective gene to its offspring.

Degenerative Myelopathy (DM)
Description:
Degenerative Myelopathy (DM) is a progressive neurological disorder that affects the spinal cord of dogs. Dogs that have inherited two defective copies can experience a breakdown of the cells responsible for sending and receiving signals from the brain, resulting in neurological symptoms.

The 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 10-12 years. However, some dogs may begin experiencing symptoms much earlier. A 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 can develop Degenerative Myelopathy, the disease does not affect every dog that has the genotype.

Test Is Relevant To the Following Breeds;

DM testing is relevant for all breeds, and is more prevalent in some breeds than others. Dogs of all breeds can be tested for DM, and is particularly recommended in the following breeds: Boxer, Chesapeake Bay Retriever, German Shepherd, Pembroke Welsh Corgi, Cardigan Welsh Corgi, Rhodesian Ridgeback, Poodle, Wire Fox Terrier, Labrador Retriever

​

Results:

Animal Genetics offers DNA testing for Degenerative Myelopathy (DM). The genetic test verifies the presence of the recessive DM mutation and presents results as one of the following:

DM/DM /At Risk/ The dog has inherited two copies of the mutated SOD1 gene and is homozygous for the mutation. The dog is at risk to develop the disorder during its lifetime. The dog will always pass a copy of the mutation to its offspring.

n/DM /Carrier/ Both the normal and mutant copies of the gene detected. Some larger dog breeds may be at risk to develop the disorder.

​
River is >  n/n > Clear >  Dog tested negative for the DM mutation and will not pass on the defective gene to its offspring.

Hyperuricosuria (HUU)

Description:
Dogs with this genetic mutation metabolize waste products as uric acid in their urine. The uric acid forms into hard stones in the bladder, causing pain and inflammation as the stone moves through the urinary tract.

A dog that has difficulty urinating or appears to have an inflamed bladder may have HUU. Other signs can include blood in the urine and frequent urination. If the dog is unable to pass the urate stones without medical intervention, surgery may be required to remove them. And if the urinary tract is blocked, the condition can be life threatening. Even in the best case scenario, HUU is uncomfortable and painful for the dog.

​
The mutation is autosomal recessive. Both parents will need to be carriers of the mutation to pass it on to their offspring. Carriers will not show any symptoms of HUU and even affected dogs may not show any signs, so it is important to test dogs for HUU prior to breeding.

Test Is Relevant to the Following Breeds:
Hyperuricosuria can be tested for in any breed, but is more prevalent in the following breeds:

All Breeds including, American Bulldog, Bulldog, French Bull Dog, American Pitbull Terrier, American Staffordshire Terrier, Australian Shepherd, Black Russian Terrier, Bulldog, Catahoula Leopard Dog, Dalmatian, German Shepherd, Giant Schnauzer, Jack Russel/Parsons Terrier, Labrador Retriever, Large Munsterlander, South African Boerboel, Vizsla and Weimaraner, Hungarian Vizsla.

Results:
Animal Genetics offers DNA testing for Hyperuricosuria. The genetic test verifies the presence of the Hyperuricosuria mutation and presents results as one of the following:

HUU/HUU    /Affected/    The dog carries two copies of the mutant gene and is homozygous for Hyperuricosuria. The dog is likely to be affected by Hyperuricosuria and will always pass a copy of the mutation to its offspring.

HUU/n /Carrier/ Both the normal and mutant copies of the gene detected. Dog is a carrier for the Hyperuricosuria mutation and can pass on a copy of the defective gene to its offspring.

River,  IS >   n/n  > Clear / Dog tested negative for the Hyperuricosuria mutation and will not pass on the defective gene to its offspring.

Juvenile Hereditary Cataracts (HSF4)

Description:
Juvenile Hereditary Cataracts (JHC) cause a clouding of the lens of the eye due to a breakdown of tissue in the eye. This condition generally results in an inability to see clearly and can cause total blindness. In canines, cataracts are often familial; this is known as Hereditary Cataracts. A mutation in the HSF4 gene causes this type of cataracts in several breeds of dogs. In this case, the dog is typically affected bilaterally. This means that both eyes are affected by the cataracts. The cataracts associated with HSF4 also occur in the posterior region of the lens. They usually start by being small and grow progressively, though the speed of growth is highly variable. Some cataracts will grow so slowly that the dog's vision remains relatively clear, while others will grow such a way that the dog will quickly go blind. Corrective surgery is possible, though it is costly and is not always effective.

​

One HSF4 mutation causes the recessive form of Juvenile Hereditary Cataracts (JHC) in Boston Terriers, Staffordshire Bull Terriers, and French Bulldogs. Because it is recessive, a dog must have two copies of this mutation to experience this form of cataracts. This mutation is only responsible for early-onset hereditary cataracts, which typically occur between 12 months and 3 years of age in Staffordshires, and between 2-3 years in Boston Terriers. Boston Terriers can also be afflicted by late-onset hereditary cataracts. However, the HSF4 gene mutation is not responsible for that particular form of cataracts. The causative gene for late-onset hereditary cataracts in Boston Terriers has not been determined at this time.
It should also be noted that not all cataracts are hereditary. Cataracts can also be caused by old age or injury. Also, cataracts that occur in different regions of the lens can also be familial, however, are not attributed to this gene mutation.

Results:
Animal Genetics offers DNA testing for the recessive JHC allele. The genetic test verifies the presence of the mutation and presents results as one of the following:

JHC/JHC    / Affected    / The dog carries two copies of the mutant gene and is homozygous for Hereditary Cataracts. The dog is affected by HSF4-Hereditary Cataracts, and will always pass on a copy of the mutated gene to its offspring.

JHC/n  / Carrier / Both the normal and mutant copies of the HSF4 gene detected. Dog is a carrier for Hereditary Cataracts, and can pass on a copy of the defective gene to any offspring.

​
River, Is  > n/n >   Clear   > Dog tested negative for the HSF4 Hereditary Cataract gene mutation, and will not pass on the defective gene to its offspring.

​

Common Symptoms -C3

Cystinuria type 3 is an inherited disease affecting kidney function in dogs. Dogs with cystinuria are deficient of a specific protein the kidneys use to transport cystine. Normal kidneys reabsorb cystine so that only small amounts pass into the urine. Dogs with cystinuria fail to reabsorb cystine, allowing large amounts to pass into the urine. Excessive cystine can form crystals and/or stones in the urinary tract, which can block the ureters or Urethra and stop the normal flow of urine. Symptoms of disease include straining to urinate, blood in the urine, frequent urination of small volumes or inability to urinate. Dogs with cystinuria often have recurrent inflammation of the urinary tract and if not treated, urinary stones can cause urinary tract infections, kidney failure and even death. Affected males are also at increased risk for urinary obstruction due to anatomical differences.

This test examines the genome for a genetic Mutation in the SLC3A1 gene associated with cystinuria type 3 (Variant 2). This mutation is not the actual mutation responsible for the disorder. It is considered a “linked marker” for cystinuria type 3. Linked markers are present in close proximity to the disease-causing mutation and are predictably inherited along with it. Making a test for the genetic mutation in the SLC3A1 gene a useful tool to assess cystinuria risk. Dogs that inherit one copy of the SLC3A1 mutation are considered carriers of the disease and will not show clinical signs of cystinuria. Cystinuria type 3 is an androgen-dependent form of the disease. Therefore, only intact males (and not females) are at an increased risk. Male dogs which inherit two copies of the SLC3A1 mutation are considered affected with cystinuria type 3 and may develop clinical signs. Although, female dogs with the SLC3A1 mutations should not develop clinical signs, they can produce at-risk/affected male offspring if bred with a dog that has also inherited these mutations.

This test also examines the genome for a genetic mutation in the SLC7A9 gene speculatively associated with cystinuria type 3 (Variant 3). This mutation is not believed to be the actual mutation responsible for the disorder. However, it may be a “linked marker” for cystinuria type 3, meaning that this marker may be present in close proximity in the genome to the mutation responsible for cystinuria type 3 and may be inherited along with the mutation which causes this disease. However, it is unconfirmed at this time if one or two copies of the SLC7A9 mutation alone is associated with cystinuria type 3.