Search Tests

Type of Test


Breeds


Disease Type


Test Name

Name SKU Price Qty Action
Ichthyosis-A (ICT-A) ICT-A $40

Ichthyosis-A (ICT-A) is a skin disease (dermatitis) seen quite commonly in Golden Retrievers that causes the outer layer of the epidermis to form improperly resulting in thick and darkened skin that becomes excessively flakey. Symptoms can exhibit a range of severity from mild itching to more severe cases involving subsequent yeast or fungal infection. The disease may be detected at an early age typically between birth and 1-2 years of age. As the dog ages symptoms may improve or worsen depending on differing stress levels, hormone cycles and diet. In some cases, scale formation has been seen to decrease in older dogs. There is no current treatment for this disease beyond standard coat care for dry skin using special shampoos and conditioners.

Papillon
Phalene

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop ICT-A nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop ICT-A but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease which results in dermatitis with symptoms of dry, flaky and discolored skin.

Name SKU Price Qty Action
Neuronal Dystrophy (NAD) NAD $40

Neuroaxonal Dystrophy (NAD) is a neurodegenerative disease that affects Papillons and Phalenes worldwide. The disease is characterized by symptoms including head tremors, wobbling gait and inability to stand or walk. Symptoms appear at a very young age usually between 1-4 months and is clinically characterized by severe axonal swelling with progression to cerebella ataxia, blindness and deafness with most dogs not surviving beyond 1 year of age.

Papillon
Phalene

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop NAD nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop NAD but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease which results in neurodegeneration and poor survival beyond 1 year of age.

Name SKU Price Qty Action
Hereditary Nasal Parakeratosis (HNPK) HNPK $40

Hereditary nasal parakeratosis (HNPK) is a disease that affects Labrador Retrievers and related breeds and leads to dry, rough, discolored crusts on the edges of the dog’s nose. The disease results from a mutation that causes the nose to dry out and can lead to chronic irritation and inflammation of the skin on and surrounding the dog’s nose. Symptoms of the disorder appear in young dogs typically between the ages of around 6 months to 1 year of age. In more severe cases of the disease, cracked skin around and on the tip of the nose can become infected and require medical attention. In later stages, the disease can also affect nose pigmentation with nose skin color changing from dark to lighter shades of color. Once diagnosed, continuous care is required to reduce the occurrence of crusting on and around the dog’s nose using topical treatments.

Labrador Retriever
Labradoodle
Australian Labradoodle

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop HNPK nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop HNPK but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease which results in discolored crusts on the edges of the dog’s nose that can become infected and require further treatment.

Name SKU Price Qty Action
Irish Setter PRA Type 1 (PRA-RCD1) PRA-RCD1 $40

Progressive retinal atrophy (PRA) in Irish Setters is an early onset inherited eye disease and can be due to more than a single mutation. One form of PRA in Irish Setters is referred to as Rod-Cone Dysplasia Type 1 (PRA-RCD1) and occurs as a result of degeneration of both rod and cone cells of the retina which are important for vision in dim and bright light. Symptoms can be recognized as early as a few weeks of age and progressive degeneration can continue for up to a year. The first signs of the disease typically present around 1 month of age with vision loss in dim light also known as night blindness. Dogs will typically show complete loss of night vision by about 5 months and difficulty with vision in bright light. Although there can be variation in disease progression, most dogs typically exhibit a rapid progression with total loss of sight by approximately 1 year of age.

Irish Setter

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop Irish Setter PRA Type 1 nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop Irish Setter PRA Type 1 and will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with Irish Setter PRA Type 1 which can result in reduced vision and total loss of sight.

Name SKU Price Qty Action
Papillon PRA Type 1 (PAP-PRA1) PAP-PRA1 $40

Progressive Retinal Atrophy (PRA) in Papillons (PAP-PRA1) is a late onset eye disorder that results in degeneration of a certain type of retinal cell which is important for low light vision. Affected dogs typically present symptoms of poor vision in dim light at approximately 4 to 6 years of age. PAP-PRA1 typically progresses slowly and can result in complete loss of vision. However, symptoms can vary with some affected dogs maintaining their daylight vision for many years and potentially the rest of their life. Ongoing research has shown that PRA in Papillons can be due to additional mutations besides the PAP-PRA1 mutation.

Papillon

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop Papillon PRA Type 1 nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop Papillon PRA Type 1 due to this particular mutation and will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with Papillon PRA Type 1 which results in vision impairment in dim light, progressive vision loss and potentially complete blindness.

Name SKU Price Qty Action
Collie Eye Anomaly (CEA) CEA $40

Collie eye anomaly (CEA) is an inherited disease that affects several dog breeds. It can also be referred to as choroidal hypoplasia (CH) due to the fact that the choroid layer of tissue is thinner in dogs suffering from the disease. This layer of tissue is responsible for supplying nutrients and blood to the retina. With insufficient blood flow the choroid does not develop properly and can often lead to retinal detachment and subsequent blindness. The disease can present itself in both a mild and severe form with symptoms varying between affected dogs. Dogs with a mild form of the disease can show thinning of the choroid and may maintain normal vision. Dogs with a more severe version of the disease can have additional eye problems leading to significant vision loss and potentially complete blindness. Although both mild and severe forms of CEA are associated with the same mutation (NHEJ1), predicting disease severity is difficult.

Aussiedoodle
Australian Shepherd
Bearded Collie
Border Collie
Boykin Spaniel
Collie
English Shepherd
Hokkaido
Lancashire Heeler
Longhaired Whippet
Miniature American Shepherd
Miniature Australian Shepherd
Nova Scotia Duck Tolling Retriever
Rough Collie
Shetland Sheepdog
Silken Windhound
Smooth Collie
Toy Australian Shepherd

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop CEA nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop CEA and will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with CEA which can result in a range of symptoms from vision impairment to complete blindness.

Name SKU Price Qty Action
Progressive Rod-Cone Degeneration (PRA-PRCD) PRA-PRCD $40

Progressive retinal atrophy (PRA) is a category of different progressive conditions related to ­retinal atrophy that can eventually lead to blindness. Progressive rod-cone degeneration (PRA-PRCD) is one specific type of PRA that affects many dog breeds. It is an inherited eye disease with late onset of symptoms that are due to degeneration of both rod and cone cells of the retina. These cells are important for vision in dim and bright light. Most dogs begin to show symptoms of the disease at approximately 3-5 years of age that manifests as difficulty seeing at night (night blindness) and loss of peripheral vision. Although rate of onset and disease progression can vary by breed, PRA-PRCD typically results in eventual loss of sight and complete blindness in affected dogs. It is important to note that other inherited eye disorders can display similar symptoms to PRA-PRCD.

American Eskimo Dog
Aussiedoodle
Australian Cattle Dog
Australian Labradoodle
Australian Shepherd
Australian Stumpy Tail Cattle Dog
Boykin Spaniel
Chesapeake Bay Retriever
Chihuahua
Chinese Crested
Cockapoo
Cocker Spaniel
English Cocker Spaniel
English Shepherd
Entlebucher Mountain Dog
Finnish Lapphund
Giant Schnauzer
Golden Retriever
Goldendoodle
Karelian Bear Dog
Kuvasz
Labradoodle
Labrador Retriever
Lapponian Herder
Markiesje
Miniature American Shepherd
Miniature Australian Shepherd
Miniature Poodle
Newfypoo
Norwegian Elkhound
Nova Scotia Duck Tolling Retriever
Poodle
Portuguese Water Dog
Schipperke
Silky Terrier
Spanish Water Dog
Standard Poodle
Swedish Lapphund
Toy Australian Shepherd
Toy Poodle
Yorkshire Terrier

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop PRA-PRCD nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop PRA-PRCD and will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with PRA-PRCD which typically results in complete blindness for most breeds.

Name SKU Price Qty Action
Von Willebrand’s Disease Type I (VWD1) VWD1 $40

Von Willebrand disease (vWD) is a genetic disorder that prevents normal blood clotting and can cause extended bleeding following injury. The disorder results from a deficiency or lack of sufficient von Willebrand factor (vWf) which functions as a binding protein during blood clotting. Three types of vWD have been identified in dogs to date and are known as vWD type 1, 2 and 3. Within these three types there are five different genetic mutations that are currently known that lead to canine vWD.

Von Willebrand’s disease type 1 (VWD1) results in reduction in normal levels of vWf to approximately 5-10% of normal. Since some vWf is produced in dogs homozygous for the VWD1 mutation, this form of the disorder is considered to be less serious than type 2 and 3. The mutation (G>A substitution) has variable penetrance and is recessive requiring two copies of the mutation in affected dogs. Typical symptoms of the disease encompass excessive or abnormal bleeding following injury or the presence of blood in various bodily secretions (urine, feces, etc.).

Bernese Mountain Dog
Coton de Tulear
Doberman Pinscher
Drentse Patrijshond
German Pinscher
Goldendoodle
Kerry Blue Terrier
Labradoodle
Manchester Terrier
Papillion
Pembroke Welsh Corgi
Poodle
Stabyhoun

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop von Willebrand’s Disease Type I disease nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop von Willebrand’s Disease Type I disease but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and are susceptible to develop problems with blood clotting.

Name SKU Price Qty Action
Pyruvate Kinase Deficiency Pug (PKD-PUG) PKD-PUG $40

Pyruvate Kinase Deficiency (PKD) is a disorder that affects red blood cells due to a mutation in an important enzyme needed for metabolism. This defect leads to red blood cell death that results in severe hemolytic anemia. Symptoms of PKD are typically exhibited between four to twelve months of age and can include weakness, lack of energy, rapid heart rate, heart murmurs, pale gums and stunted growth. With further progression, bones and the liver can be affected ultimately leading to death. Dogs with PKD commonly die before the age of 4 years but longevity can vary based on the breed of dog with some breeds able to survive longer than others. While there is currently no cure for PKD, it is possible for affected dogs to have a reasonable quality of life with the proper care. Carrier dogs do not typically show symptoms of the disease and it may be difficult to detect clinical signs of the condition in inactive affected dogs so it is useful to test for the presence of the mutation before breeding. PKD was originally documented in Basenjis and has since been reported in other breeds, including Dachshunds, Labrador Retrievers, Pugs, Beagles, Cairn Terrier and West Highland White Terriers. There are a number of mutations leading to PKD and are different based on breed. When choosing a test, please select the mutation appropriate for your breed.

Pug (PKD-PUG)

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop PKD nor pass this mutation to their offspring.

Name SKU Price Qty Action
Pyruvate Kinase Deficiency Labrador Retriever (PKD-LAB) PKD-LAB $40

Pyruvate Kinase Deficiency (PKD) is a disorder that affects red blood cells due to a mutation in an important enzyme needed for metabolism. This defect leads to red blood cell death that results in severe hemolytic anemia. Symptoms of PKD are typically exhibited between four to twelve months of age and can include weakness, lack of energy, rapid heart rate, heart murmurs, pale gums and stunted growth. With further progression, bones and the liver can be affected ultimately leading to death. Dogs with PKD commonly die before the age of 4 years but longevity can vary based on the breed of dog with some breeds able to survive longer than others. While there is currently no cure for PKD, it is possible for affected dogs to have a reasonable quality of life with the proper care. Carrier dogs do not typically show symptoms of the disease and it may be difficult to detect clinical signs of the condition in inactive affected dogs so it is useful to test for the presence of the mutation before breeding. PKD was originally documented in Basenjis and has since been reported in other breeds, including Dachshunds, Labrador Retrievers, Pugs, Beagles, Cairn Terrier and West Highland White Terriers. There are a number of mutations leading to PKD and are different based on breed. When choosing a test, please select the mutation appropriate for your breed.

Labrador Retriever (PKD-LAB)

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop PKD nor pass this mutation to their offspring.

Name SKU Price Qty Action
Pyruvate Kinase Deficiency Beagle (PKD-BEA) PKD-BEA $40

Pyruvate Kinase Deficiency (PKD) is a disorder that affects red blood cells due to a mutation in an important enzyme needed for metabolism. This defect leads to red blood cell death that results in severe hemolytic anemia. Symptoms of PKD are typically exhibited between four to twelve months of age and can include weakness, lack of energy, rapid heart rate, heart murmurs, pale gums and stunted growth. With further progression, bones and the liver can be affected ultimately leading to death. Dogs with PKD commonly die before the age of 4 years but longevity can vary based on the breed of dog with some breeds able to survive longer than others. While there is currently no cure for PKD, it is possible for affected dogs to have a reasonable quality of life with the proper care. Carrier dogs do not typically show symptoms of the disease and it may be difficult to detect clinical signs of the condition in inactive affected dogs so it is useful to test for the presence of the mutation before breeding. PKD was originally documented in Basenjis and has since been reported in other breeds, including Dachshunds, Labrador Retrievers, Pugs, Beagles, Cairn Terrier and West Highland White Terriers. There are a number of mutations leading to PKD and are different based on breed. When choosing a test, please select the mutation appropriate for your breed.

Beagle

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop PKD nor pass this mutation to their offspring.

Name SKU Price Qty Action
Benign Familial Juvenile Epilepsy (BFJE) BFJE $40

Benign Familial Juvenile Epilepsy (BFJE) is an inherited neurological disease that occurs in Lagotto Romagnolo dogs due to a mutation in the LGI2 gene. Symptoms of BFJE typically occur early in pups between five to nine weeks of age and are characterized by seizures that usually resolve by approximately four months of age but some adult cases of BFJE have been observed within the breed. Severely affected dogs may develop ataxia in addition to seizures. With disease resolution, the prognosis for affected dogs is typically good.

Lagotto Romagnolo

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop BFJE nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop BFJE and will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with BFJE which results in seizures and potential ataxia.

Name SKU Price Qty Action
Coat Length/Fluffy Locus (LENGTH) LENGTH $40

The length of a dog’s coat can vary between breeds with some breeds typically showing short haired coats and other breeds showing long haired coats. It has been determined that hair length variation is due to a mutation in the FGF5 gene that changes the hair follicle growth termination signal which impacts canine hair length. The mutation is recessive which means a dog must have two copies of the mutation that will typically result in a long or fluffy coat.

All breeds

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop long hair nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this trait. They will not develop long hair and will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with long hair which results in a long-haired coat.

Name SKU Price Qty Action
Curly Coat Locus (CURL) CURL $40

Hair curl is an incomplete dominant characteristic caused by a mutation in the KRT71 gene. Incomplete dominance refers to the fact that a dog can carry one copy of the gene which will result in a moderately curly (known as “wavy”) coat or two copies of the mutation which will result in a tightly curled coat. Dogs lacking the mutation will typically have straight hair. This particular mutation can be found prevalently in some breeds that typically display a curly coat. The hair curl mutation can also be accompanied by the other mutations such as coat length and furnishings that can also contribute to the overall look of a dog’s coat.

Airedale Terrier
American Water Spaniel
Bichon Frise
Border Collie
Boykin Spaniel
Chesapeake Bay Retriever
Chihuahua
Dachshund
Havana Silk Dog
Havanese
Kerry Blue Terrier
Kuvasz
Leonberger
Maltese
Pharaoh Hound
Portuguese Water Dog
Soft-Coated Wheaten Terrier
Welsh Terrier
Wire Fox Terrier

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will have straight hair.

B (CARRIER/AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with a curly coat type. Due to incomplete dominant expression, these dogs can have a “wavy” or moderately curly coat that is in the spectrum somewhere between a curly and a straight coat. They will also if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation which typically results in a tight curly coat.

 

Name SKU Price Qty Action
Dominant PRA (PRA-D) PRA-D $40

Dominant PRA is an eye disorder that affects English Mastiffs and Bull Mastiffs. It is a form of progressive retinal atrophy (PRA) that causes cells of the eye to deteriorate over time eventually leading to complete blindness. Typically, affected dogs show symptoms of the disease starting at approximately 2-3 years of age however, symptoms including night-blindness have been observed in puppies as young as 6 weeks. Progression of the disease is fairly quick with most affected dogs suffering complete blindness within 1-2 years from the onset of symptoms. This particular type of PRA seen in the Mastiff breeds is a dominant condition which means a dog only need inherit one copy of the mutation to be affected by the disease.

English Mastiff
Bullmastiff

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop PRA-D nor pass this mutation to their offspring.

B (CARRIER/AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will develop PRA-D and will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with PRA-D which results in visual deterioration and eventual blindness.

Name SKU Price Qty Action
D Locus (D-LOCUS) D-LOCUS $40

The MLPH gene codes for a protein called melanophilin, which is responsible for transporting and fixing melanin-containing cells. A mutation in this gene leads to improper distribution of these cells, causing a dilute coat color. This mutation is recessive so two copies of the mutated gene (or “d” allele) are needed to produce the dilute coat color. This mutation affects both Eumelanin and Pheomelanin pigments, so black, brown and yellow dogs are all affected by the dilution with the effect being more pronounced in black dogs. The mutation responsible for the dilution phenotype is recessive so a dog can be a carrier of the dilution gene and still appear to have a normal coat color. A diluted yellow (ee) dog is often referred to as a champagne.

All breeds

A (CLEAR/NORMAL): These dogs have two copies of the normal gene, will have an undiluted coat and will not pass the mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with dilute coat coloring. They will have an undiluted coat but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the MLPH mutation associated with a diluted coat color which results in blue, charcoal, grey, lilac or champagne coat dependent on other coat color loci.

Name SKU Price Qty Action
E Locus (E-LOCUS) E-LOCUS $40

A mutation in the MC1R gene (E locus) is responsible for the presence of yellow to red coats in many different domestic dog breeds. The dominant non-mutated form of the gene (“E” allele) allows the dog to produce a black pigment called Eumelanin. A mutation in the MC1R gene causes the pigment-producing cells to generate a yellow pigment called Pheomelanin. A dog must have two copies of the MC1R recessive mutation (represented as the “e” allele) to express the solid yellow coat color. This “ee” genotype can vary in expression ranging from yellow or red coloring to more subtle differences (apricot, cream or white) depending on the breed.

All breeds

A (CLEAR/NORMAL): These dogs have two copies of the normal gene, will have a black-based coat and will not pass the mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with yellow to red coloring. They will have a black-based coat but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the MC1R mutation associated with a yellow coat which results in a yellow to red coat coloring that varies by breed.

Name SKU Price Qty Action
Trapped Neutrophil Syndrome (TNS) TNS $40

The mutation causes the dog’s infection-fighting white blood cells to be “trapped” and not released from the bone marrow. Without sufficient white blood cells in the bloodstream, the dog’s immune system is unable to fight off infections and the dog eventually dies, usually when they are a few months old. An affected puppy may not show any specific symptoms, other than susceptibility to infection, but may be smaller and less healthy than unaffected puppies. Occasionally, a dog will not show symptoms until they are older, around 7 months old. There is currently no treatment for TNS. However, the infections can be treated with antibiotics or steroids to prolong the life of the dog. It is estimated that about 10% of Border Collies are carriers of the mutation, so testing for TNS before breeding is advisable.

Border Collies

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop Papillon PRA Type 1 nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop Papillon PRA Type 1 due to this particular mutation and will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with Papillon PRA Type 1 which results in vision impairment in dim light, progressive vision loss and potentially complete blindness.

Name SKU Price Qty Action
SOD1B Degenerative Myelopathy (SOD1B) SOD1B $40

Degenerative Myelopathy (DM) is a progressive disease of the spinal cord in older dogs. In many breeds, the disease is strongly correlated with a mutation in the superoxide dismutase 1 (SOD1) gene often referred to as the 118G>A mutation. This mutation is tested for using the standard DM test (see above). More recently, a second mutation in the SOD1 gene has been detected in the Bernese Mountain Dog (BMD) and is referred to as the SOD1B 52A>T mutation. To date, a single BMD with two copies of the 52A>T mutation and no copies of the 118G>A mutation has been clinically diagnosed with DM. In one additional study, a single BMD that tested ‘CARRIER’ for both the 118G>A and the 52A>T showed clinical signs of DM highlighting the potential for complex mutation interactions.

The SOD1B mutation is detected much less frequently (3%) than the 118G>A mutation (38%) in BMD but could play a role in disease progression. In an effort to further understand the disease in the breed, the SOD1B test is being offered. Please share the results in an open database such as The Berner-Garde Foundation (http://www.bernergarde.org/home/), a group established to collect, maintain and disseminate information about genetic diseases observed in the BMD. Through tracking of the health and SOD1B status, a better understanding of the impact of this mutation on the breed can be determined.

Bernese Mountain Dog

A (CLEAR/NORMAL): These dogs have two normal copies of DNA. To date, no dogs tested as ‘CLEAR/NORMAL’ have been confirmed to have DM.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the 52A>T mutation and one normal copy of DNA. One compound carrier (118G>A carrier, 52A>T) to date has been confirmed to have DM.

C (AT RISK/AFFECTED): These dogs have two copies of the 52A>T mutation and may develop DM during their lifetime. At this point, the SOD1B mutation can be interpreted as being ‘AT RISK’ of developing DM within the animal’s lifetime. For dogs showing clinical signs with a presumptive diagnosis of DM, ‘AT RISK/AFFECTED’ test results can be used as an additional tool to aid in the diagnosis of DM.

Name SKU Price Qty Action
Primary Lens Luxation (PLL) PLL $40

The lens of the eye normally lies immediately behind the iris and the pupil, and is suspended in place by a series of fibers. It functions to focus light rays on the retina, in the back of the eye. When partial or complete breakdown of these fibers occur, the lens may become partially or fully dislocated from its normal position. Lens luxation can occur for several different reasons. Primary lens luxation is a heritable disease in many breeds and spontaneous luxation of the lens occurs in early adulthood (most commonly 3-6 years of age) and often affects both eyes, although not necessarily at the same time. Lens luxation can lead to inflammation and glaucoma that can result in painful, teary, red eyes that may look hazy or cloudy. If detected early, surgical removal of the lens can be beneficial. Medical treatment of inflammation and glaucoma in the form of topical and oral medications can relieve much of the discomfort associated with this disease.

American Eskimo Dog
American Hairless (Rat) Terrier
Australian Cattle Dog
Chinese Crested
Chinese Foo Dog
Jack Russell Terrier
Jagd Terrier
Lakeland Terrier
Lancashire Heeler
Lucas Terrier
Miniature Bull Terrier
Norfolk Terrier
Norwich Terrier
Parson Russell Terrier
Rat Terrier
Russell Terrier
Sealyham Terrier
Tenterfield Terrier
Tibetan Terrier
Toy Fox Terrier
Volpino Italiano
Welsh Terrier
Yorkshire Terrier
Hybrid/Mix-Breed

A (CLEAR/NORMAL): These dogs have two normal copies of DNA. Research has demonstrated clear dogs will not develop PLL as a result of the mutation, although it is possible they might develop PLL due to other causes, such as trauma or the effects of other, unidentified mutations.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the mutation and one normal copy of DNA. Research has demonstrated that carriers have a very low risk of developing PLL. The majority of carriers do not develop PLL during their lives but a small percentage do. Current estimates are that between 2% – 20% of carriers will develop the condition.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation and will almost certainly develop PLL during their lifetime. It is advised that all genetically affected dogs have their eyes examined by a veterinary ophthalmologist every 6 months, from the age of 18 months, so the clinical signs of PLL are detected as early as possible.

Name SKU Price Qty Action
Primary Hyperoxaluria (PH) PH $40

Primary Hyperoxaluria (PH) is a metabolic disorder that affects the Coton de Tulear dog breed. The disease results from a liver enzyme deficiency required to break down calcium oxalate crystals so they can be eliminated from a dog’s system. Without a properly functioning enzyme, crystals build up in the dog’s body leading to progressive illness. Affected puppies show signs of the disorder at 3-4 weeks of age with the disease eventually leading to kidney failure. Symptoms of acute renal failure can include loss of appetite, vomiting, lethargy, decreased urine production, abdominal pain and blood in the urine. PH affected puppies rarely survive beyond a few months. This test includes PH1.

Coton de Tulear

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop PH nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop PH but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease which results in eventual kidney failure and poor survival beyond a few weeks of age.

Name SKU Price Qty Action
Phosphofructokinase Deficiency (PFK) PFK $40

Canine Phosphofructokinase Deficiency (PFK) is a genetic disease which prevents the metabolism of glucose into available energy resulting in exercise intolerance and muscle disease in Cocker Spaniels. PFK deficiency also destroys red blood cells in affected dogs, leading to anemia. The PFK deficiency gene frequency in Cockers is estimated to be 2-10% of the population.

American Cocker Spaniel
Cocker Spaniel
English Cocker Spaniel
English Springer Spaniel
Whippet

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop PFK disorder nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop PFK disorder but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and are susceptible to develop exercise intolerance and muscle disease.

Name SKU Price Qty Action
Newfoundland Cystinuria (CYS) CYS $40

Cystinuria in the Newfoundland dog is indicated by the presence of cystine stones in the kidney, bladder or ureter. Failure by the kidneys to reabsorb amino acids results in the formation of these stones. In this disorder, the kidneys do not adequately reabsorb certain amino acids during the filtering process, thus resulting in excess excretion of these amino acids. The amino acids may precipitate and form crystals or stones in the kidneys, ureters, or bladder.

Newfoundland

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop cystine stone disorder nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop cystine stone disorder but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and are susceptible to develop bladder/kidney stones.

Name SKU Price Qty Action
Neonatal Encephalopathy (NE) NE $40

Neonatal encephalopathy (NE) or Neonatal encephalopathy with seizures (NEwS) is a recessive developmental brain disease. Affected pups exhibit extreme weakness, and those that survive the first week generally develop progressively worse ataxia, or inability to move properly. This is often accompanied by severe seizures. None have survived to 7 weeks of age.

Goldendoodle
Labradoodle
Standard Poodle

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop NE nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop NE but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and which results in ataxia and poor survival beyond 7 weeks of age.

Name SKU Price Qty Action
Multidrug Sensitivity (MDR1) MDR1 $40

The MDR1 gene, or multi-drug resistance gene, codes for a protein that is responsible for protecting the brain by transporting potentially harmful chemicals away from the brain. In certain breeds, a mutation occurs in the MDR1 gene that causes sensitivity to Ivermectin, Loperamide, and a number of other drugs. Dogs with this mutation have a defect in the P-glycoprotein that is normally responsible for transporting certain drugs out of the brain. The defective protein inhibits the dog’s ability to remove certain drugs from the brain, leading to a buildup of these toxins. As a result of accumulation of toxins, the dog can show neurological symptoms, such as seizures, ataxia, or even death. Dogs that are homozygous for the MDR1 gene, meaning that they have two copies of the mutation, will display a sensitivity to Ivermectin, and other similiar drugs. Dogs that are heterozygous, meaning they have only one copy of the mutation, can still react to these drugs at higher doses.

Australian Shepherd
Border Collie
Collie
English Shepherd
German Shepherd
Long-haired Whippet
McNab
Old English Sheepdog
Shetland Sheepdog
Silken Windhound

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop MDR1 nor pass this mutation to their offspring.

B (CARRIER/AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They can react to certain drugs at higher doses and pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and which results in sensitivity to a number of drugs including but not limited to Ivermectin, Loperamide, Doxorubicin, Cyclosporin, Digoxin, Acepromazine, Butorphanol and others.

Name SKU Price Qty Action
Labrador Centronuclear Myopathy (CNM) CNM $40

Centronuclear myopathy in Labrador Retrievers is a recessively-inherited muscular disease. This disease was previously known as Labrador muscular myopathy. The disease is characterized by early onset muscular problems such as awkward gait, fatigue, and difficulty eating. Puppies are born apparently normal; however, it quickly becomes evident that there is problem. The puppy will often not gain weight adequately, due to decreased muscle tone in the esophagus. Within 2 to 5 months, the disease has usually progressed to display the full range of symptoms. This condition is exacerbated in cold conditions. Unfortunately, there is no cure for CNM, as the dog will never develop properly functioning muscle tissue. The dog usually has a normal life span, however, he will always be plagued with the symptoms.

Labrador Retriever

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop CNM nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop CNM but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and are susceptible to develop insufficient muscle function.

Name SKU Price Qty Action
Hyperuricosuria (HU) HU $40

This disease is characterized by the excretion of uric acid leading to the formation of urinary calculi (stones) which may then require surgery. If a dog from a breed susceptible to this disorder is seen to experience problems urinating freely, then veterinary advice should be sought immediately.

American Staffordshire Terrier
Australian Shepherd
Black Russian Terrier
Bulldog
Coton De Tulear
Dalmatian
German Shepherd Dog
Giant Schnauzer
Jack Russell/Parsons Terrier
Large Munsterlander
Pitbull
South African Boerboel
Weimaraner
All breeds

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop urate stone disorder nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop urate stone disorder but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and are susceptible to develop bladder/kidney stones.

Name SKU Price Qty Action
Hereditary Cataracts (HC) HC $40

Cataracts are a clouding of lens of the eye caused by a breakdown of tissue in the eye. This generally results in an inability to see clearly, and can cause total blindness. In canines, mutations that result in cataracts can be passed to offspring and is known as Hereditary Cataracts (HC), Juvenile Cataracts (JC) or Early Onset cataracts (EOC). 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 with both eyes affected by the disease. The cataracts associated with HSF4 also occur in the posterior region of the lens. They usually begin 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 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 HC 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 HC, 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 HC; however, the HSF4 gene mutation is not responsible for that particular form of cataracts. A separate mutation of the HSF4 gene is responsible for HC in Australian Shepherds. This mutation affects Aussies differently, in that the disease is dominant, but not completely penetrant. This means that only one copy of the mutation is necessary to predispose a dog to the disease, however, incomplete penetrance means that a dog that has this mutation will not always develop HC. Research suggests that the mutation makes a dog 12 times more likely to develop posterior bilateral cataracts at some point in their lifetime. It is likely that a secondary gene interaction occurs in the small percentage of dogs possessing the HC mutation but do not develop cataracts, however, this interaction is not yet know. It is important to note 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, but not necessarily attributed to this gene mutation.

Australian Shepherd
Boston Terrier
French Bulldog
Staffordshire Bull Terrier

Terrier and Bulldog:

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop HSF4-Hereditary Cataracts nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop HC but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs carries two copies of the mutant gene and are homozygous for HC. The dog is affected by HSF4-Hereditary Cataracts, and will always pass on a copy of the mutated gene to its offspring.

Australian Shepherd:

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop HSF4-Hereditary Cataracts nor pass this mutation to their offspring.

B (CARRIER/AT RISK): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will likely develop HC and will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs carries two copies of the mutant gene and are homozygous for HC. The dog will very likely be affected by HSF4-Hereditary Cataracts, and will always pass on a copy of the mutated gene to its offspring.

Name SKU Price Qty Action
Exercise Induced Collapse (EIC) EIC $40

Exercise Induced Collapse (EIC) is a canine genetic disorder that leads to loss of muscle control following periods of extreme exercise. Episodes generally occur after 5-25 minutes of excessive activity that can include actively running for extended periods of time. Episode severity ranges between different dogs and often begins with a form of rocking followed by weakening of the hind limbs and eventual collapse. Attacks are typically brief (less than 20 minutes) and dogs tend to recover. In a limited number of cases, episodes can be fatal. Affected dogs begin to show symptoms from a couple of months to 3 years of age and are more susceptible at an age when more intensive training begins. It is important for owners of dogs affected with EIC to be familiar with activities that may trigger an episode.

Boykin Spaniel
Bouvier des Flanders
Chesapeake Bay Retriever
Cocker Spaniels
Curly-Coated Retriever
German Wirehaired Pointer
Labrador Retriever
Old English Sheepdogs
Pembroke Welsh Corgi

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop Exercise Induced Collapse nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop Exercise Induced Collapse but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and are susceptible to collapse following periods of extreme exercise.

Name SKU Price Qty Action
Collie Cyclic Neutropenia (CN) CN $40

This disorder, also known as ‘gray collie syndrome,’ is characterized by a reduced number of neutrophils which drops dramatically in a cyclical pattern, usually about every 10 to 12 days. During the time of a low neutrophil count, there is an increased susceptibility to infection. Affected dogs develop clinical signs such as fever, diarrhea, joint pain, or other signs associated with eye, respiratory, or skin infections. They are also prone to bleeding episodes. This is a serious genetic disorder in which affected puppies are smaller and weaker, with a noticeable pale gray or pinkish/gray or beige color. These puppies rarely live beyond a couple of days and when they do survive, they are susceptible to a number of infections. With proper treatment they can be kept alive, but few have lived beyond 2 to 3 years of age.

Border Collie
Collie

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop CN nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop CN but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and which results in a reduced white cell count and increased susceptibility to infection.

Name SKU Price Qty Action
Canine Multifocal Retinopathy (CMR2) CMR2 $40

The canine multifocal retinopathy mutation causes raised lesions to form on the retina which alters the appearance of the eye but usually does 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. The genetic test for CMR is valuable for identifying the cause of a retinal deformation. Given the exact genetic diagnosis, the owner can be reassured that there probably will be little or no vision loss due to this condition.

While both CMR1 and CMR2 mutations are in the same gene, they are breed specific and testing for only one is required. The CMR2 mutation is specific for the Coton de Tulear breed. All other breeds listed should test for the CMR1 mutation.

Coton de Tulear

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop CMR disorder nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop CMR disorder but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and are susceptible to develop retinal deformation.

Name SKU Price Qty Action
Canine Multifocal Retinopathy (CMR1) CMR1 $40

The canine multifocal retinopathy mutation causes raised lesions to form on the retina which alters the appearance of the eye but usually does 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. The genetic test for CMR is valuable for identifying the cause of a retinal deformation. Given the exact genetic diagnosis, the owner can be reassured that there probably will be little or no vision loss due to this condition.

While both CMR1 and CMR2 mutations are in the same gene, they are breed specific and testing for only one is required. The CMR2 mutation is specific for the Coton de Tulear breed. All other breeds listed should test for the CMR1 mutation.

American Bulldogs
Australian Shepherds
Bullmastiffs
Cane Corsos
Dogue de Bordeaux
English Bulldogs
English Mastiffs
Great Pyrenees
Perro de Presa Canario

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop CMR disorder nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop CMR disorder but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and are susceptible to develop retinal deformation.

Name SKU Price Qty Action
Canine Factor VII Deficiency (CFVII) CFVII $40

Factor VII is a clotting factor synthesized in the liver that is necessary to initiate blood coagulation when vascular injury occurs. The condition is not fatal but can cause increased bleeding after surgery or injury in affected dogs. In rare circumstances, an affected dog may experience excessive bleeding and require a blood transfusion.

Airedale
Alaskan Klee Kai
Beagle
Giant Schnauzer
Scottish Deerhound

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop factor VII deficiency nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop factor VII deficiency but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease and are susceptible to develop problems with blood clotting.

Name SKU Price Qty Action
Canine Degenerative Myelopathy (DM) DM $40

Degenerative Myelopathy (DM) is a progressive disease of the spinal cord in older dogs. The disease has an insidious onset typically between 8 and 14 years of age. It begins with a loss of coordination (ataxia) in the hind limbs. The affected dog will wobble when walking, knuckle over or drag the feet. This can first occur in one hind limb and then affect the other. As the disease progresses, the limbs become weak and the dog begins to buckle and has difficulty standing. The weakness gets progressively worse until the dog is unable to walk. The clinical course can range from 6 months to 1 year before dogs become paraplegic. If signs progress for a longer period of time, loss of urinary and fecal continence may occur and eventually weakness will develop in the front limbs. Another key feature of DM is that it is not a painful disease. Although any dog can be tested for DM, it is possible that the genetic background that predominates in some breeds prevents the development of symptoms even in dogs testing affected (at risk). At this time the required evidence of association between the genetic mutation and actual spinal cord evaluations has only been proven in the breeds listed.

Please see http://www.offa.org/dnatesting/dmexplanation.html and http://www.caninegeneticdiseases.net/DM/ancmntDM.htm for additional information on DM diagnosis.

American Eskimo Dogs
Australian Shepherds
Bernese Mountain Dog
Borzoi
Boxers
Cardigan Welsh Corgi
Chesapeake Bay Retrievers
Coton De Tulear
German Shepherd Dog
Golden Retriever
Great Pyrenees
Irish Setters
Kerry Blue Terriers
Pembroke Welsh Corgis
Poodle
Pug
Rhodesian Ridgeback
Shetland Sheepdog
Soft Coated Wheaten Terriers
Wire Fox Terrier

A (CLEAR/NORMAL): These dogs have two normal copies of DNA. Among the hundreds of dogs studied to date at the University of Missouri, only two dogs with test results of ‘CLEAR/NORMAL’ have been confirmed to have DM.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the mutation and one normal copy of DNA. Carriers are far less likely to develop DM however; a few cases to date of DM have been confirmed in a small number of carrier dogs.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation and will likely develop DM during their lifetime. Although many dogs tested to date typed as ‘AT RISK/AFFECTED’ have been clinically confirmed DM, recent evidence suggest that there are other causes of DM in some breeds. In addition, not all dogs testing as ‘AT RISK/AFFECTED’ have shown clinical signs of DM. Research is ongoing to estimate what percentage of dogs testing as ‘AT RISK/AFFECTED’ will develop DM within their lifespan. At this point, the DM mutation can be interpreted as being ‘AT RISK’ of developing DM within the animal’s lifetime. For dogs showing clinical signs with a presumptive diagnosis of DM, ‘AT RISK/AFFECTED test results can be used as an additional tool to aid in the diagnosis of DM.

Name SKU Price Qty Action
Bandera’s Neonatal Ataxia (BNAT) BNAT $40

Bandera’s Neonatal Ataxia (also referred to as Bandera’s Syndrome) is a hereditary disease found only in the Coton de Tulear dog. This hereditary disease is named for the second Coton puppy diagnosed with the disease and results in affected puppies with an inability to coordinate their movements. This is due to a mutation in a glutamate receptor gene that affects neurotransmitter levels leading to improper brain signals and impeded movement coordination. Affected puppies can be recognized within the first few weeks as displaying difficulties walking, eating, standing and eliminating. There have been no known adult Cotons affected with Bandera’s Neonatal Ataxia.

Coton de Tulear

A (CLEAR/NORMAL): These dogs have two copies of the normal gene and will neither develop BNAT nor pass this mutation to their offspring.

B (CARRIER/NOT AFFECTED): These dogs have one copy of the normal gene and one copy of the mutation associated with this disease. They will not develop BNAT but will, if bred, pass the mutation to 50% of its offspring, on average.

C (AT RISK/AFFECTED): These dogs have two copies of the mutation associated with this disease which results in ataxia and poor survival beyond a few weeks of age.