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Collie DNA Bundle: CEA Option 1 + DM exon2 + HUU (SLC) + MDR1 + rcd2-PRA
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1 ) Collie Eye Anomaly (CEA) / Choroidal Hypoplasia (CH) Option 1*
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Re ISDS: Please note that this test is accepted by the ISDS provided that the sample is collected by a vet who should also sign a sample collection form which can be downloaded from the following link: ISDS DNA Bundle Order Form '
Kennel Club: results of this test is accepted by the Kennel Club
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Breeds
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Australian Shepherd
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Bearded Collie
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Border collie
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Boykin Spaniel
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English shepherd
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Hokkaido
,
Lancashire Heeler
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Longhaired Whippet
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Miniature American Shepherd
,
Nova Scotia Duck tolling Retriever ( NSDTR )
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Rough Collie
,
Shetland Sheepdog (Sheltie)
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Silken Windhound
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Smooth Collie
,
Long Haired Whippet
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Kennel Club
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This test is part of the Official UK Kennel Club DNA Testing Scheme in Australian Shepherd , Bearded Collie , Border collie , Lancashire Heeler , Nova Scotia Duck tolling Retriever ( NSDTR ) , Rough Collie , Shetland Sheepdog (Sheltie) , and Smooth Collie.
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The Disease |
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Collie Eye Anomaly is an inherited disease with recessive mode of inheritacne which results in abnormal development of the eye's choroid.The disease can be mild or servere, in the mild form of the disease, there is a thinning in the choroid layer of the eye but the dog's vision remains normal, however, dogs with the mild form of the disease can produce severly afected offspring.
In the Severe form of the disease, the dog can suffer serious loss of vision, Colobomas can be seen around and at the optic nerve head as outpouchings in the eye tissue layers. Colobomas may lead to secondary complications such as partial or complete retinal detachments and/or growth of new but abnormal blood vessels with bleeding inside the eye. The disease can affect one or both eyes and can lead to vision loss although this disease rarely lead to complete blindness.
* test performed by partner lab
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Trait of Inheritance |
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Inheritance : AUTOSOMAL
RECESSIVE
trait
Sire
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Dam
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Offspring
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clear
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clear
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100% clear
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clear
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carrier
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50% clear + 50%
carriers
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clear
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affected
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100% carriers
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carrier
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clear
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50% clear + 50%
carriers
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carrier
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carrier
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25% clear + 25% affected
+ 50% carriers
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carrier
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affected
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50% carriers + 50%
affected
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affected
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clear
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100% carriers
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affected
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carrier
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50% carriers + 50%
affected
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affected
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affected
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100% affected
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Clear
Genotype: N / N [ Homozygous normal ]
The dog is noncarrier of the mutant gene.
It is very unlikely that the dog will develop Collie Eye Anomaly (CEA) / Choroidal Hypoplasia (CH) Option 1*. The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.
Carrier
Genotype: N / CEA [ Heterozygous ]
The dog carries one copy of the mutant gene and one
copy of the normal gene.
It is very unlikely that the dog will develop Collie Eye Anomaly (CEA) / Choroidal Hypoplasia (CH) Option 1* but since it carries the mutant gene, it can pass it on to its offspring with the probability of 50%. Carriers should only be bred to clear dogs. Avoid breeding carrier to carrier because 25% of their offspring is expected to be affected (see table above)
Affected
Genotype: CEA / CEA [ Homozygous mutant ]
The dog carries two copies of the mutant gene and
therefore it will pass the mutant gene to its entire offspring.
The dog is likely to develop Collie Eye Anomaly (CEA) / Choroidal Hypoplasia (CH) Option 1* and will pass the mutant gene to its entire offspring
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Sample Requirements |
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Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs.
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
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2 ) Degenerative Myelopathy / Degenerative Radiculomyelopathy) DM (Exon 2)
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Breeds
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Airedale Terrier
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Alaskan Malamute
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All Dog Breeds
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American Eskimo
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Bernese Mountain Dog
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Bloodhound
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Borzoi (Russian Wolfhound)
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Boxer
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British Timber Dog
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Cavalier King Charles Spaniel
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Canaan Dog
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Cardigan Welsh Corgi
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Chesapeake Bay Retriever
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Fox Terrier
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French Bull Dog
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German Shepherd
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Glen Of Imaal Terrier
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Golden Retriever
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Pyrenean Mountain Dog (Great Pyrenees)
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Hovawart
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Hungarian Pumi
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Jack Russell Terrier
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Kerry Blue Terrier
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Labrador Retriever
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Lakeland Terrier
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Northern Inuit
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Nova Scotia Duck tolling Retriever ( NSDTR )
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Pembroke Welsh Corgi
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Poodle
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Pug
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Rhodesian Ridgeback
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Rough Collie
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Soft Coated Wheaten Terrier
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Shetland Sheepdog (Sheltie)
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Smooth Collie
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Utonagan
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Wire Fox Terrier
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Kennel Club
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This test is part of the Official UK Kennel Club DNA Testing Scheme in Chesapeake Bay Retriever , French Bull Dog , German Shepherd , Nova Scotia Duck tolling Retriever ( NSDTR ) , Rough Collie , and Smooth Collie.
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The Disease |
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Canine degenerative myelopathy (also known as chronic degenerative radiculomyelopathy) is a progressive disease of the spinal cord in older dogs. The disease has an insidious onset typically between 7 and 14 years of age. It begins with a loss of coordination (ataxia) in the hind limbs. As of July 15, 2008 the mutated gene responsible for DM has been found present in 43 breeds including German Shepherds, Boxers, Chesapeake Bay Retrievers, Rhodesian Ridgebacks, and both breeds of Welsh Corgis. The disease is chronic and progressive, and resulting in paralysis.
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Clinical Signs |
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Degenerative myelopathy initially affects the back legs and causes muscle weakness and loss, and lack of coordination. These cause a staggering effect that may appear to be arthritis. The dog may drag one or both rear paws when it walks. This dragging can cause the nails of one foot to be worn down. The condition may lead to extensive paralysis of the back legs. As the disease progresses, the animal may display symptoms such as incontinence and has considerable difficulties with both balance and walking. If allowed to progress, the animal will show front limb involvement and extensive muscle atrophy. Eventually cranial nerve or respiratory muscle involvement necessitates euthanasia.
Progression of the disease is generally slow but highly variable. The animal could be crippled within a few months, or may survive up to three years
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Trait of Inheritance |
Tow alleles are invloved in Degenerative Myelopathy, A and G, therefore a test result can be A/A, A/G, or G/G.
Mode of inheritance is autosomal recessive with variable penetrance;
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Inheritance : AUTOSOMAL
RECESSIVE
trait
Sire
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Dam
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Offspring
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clear
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clear
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100% clear
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clear
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carrier
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50% clear + 50%
carriers
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clear
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affected
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100% carriers
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carrier
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clear
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50% clear + 50%
carriers
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carrier
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carrier
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25% clear + 25% affected
+ 50% carriers
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carrier
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affected
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50% carriers + 50%
affected
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affected
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clear
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100% carriers
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affected
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carrier
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50% carriers + 50%
affected
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affected
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affected
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100% affected
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Clear
Genotype: N / N [ Homozygous normal ]
The dog is noncarrier of the mutant gene.
It is very unlikely that the dog will show signs of the Degenerative Myelopathy
Carrier
Genotype: N / DM (Exon 2) [ Heterozygous ]
The dog carries one copy of the mutant gene and one
copy of the normal gene.
It is very unlikely that the dog will show signs of the Degenerative Myelopathy
Affected
Genotype: DM (Exon 2) / DM (Exon 2) [ Homozygous mutant ]
The dog carries two copies of the mutant gene and
therefore it will pass the mutant gene to its entire offspring.
The dog may or may not show signs of the disease
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Sample Requirements |
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Buccal Swabs or 0.5 - 1 ml blood in EDTA Blood Tube
Buccal swabs or 0.5 - 1 ml blood in EDTA Blood Tube .
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3 ) Hyperuricosuria / Urate Stones (HUU, SLC)
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New Kennel Club DNA testing scheme for HUU in Dalmatian |
The Kennel Club has agreed a new DNA testing scheme for Hyperuricosuria (HUU) / Urate Stone Disorder (USD) in Dalmatian. Under this scheme, HUU test results can be sent by Laboklin to the Kennel Club to be recorded and published only if the submission and testing procedure complies with the following protocol:
- that dogs to be tested are microchipped and registered before the test sample is taken;
- that the test sample (whether buccal swab or EDTA blood sample or other) is taken by a veterinary surgeon or veterinary nurse who first confirms the microchip identity of the test subject and records both the microchip number and registration name on the sample container/package;
- that the sample is sent directly by the veterinary surgery to LABOKLIN.
Copies of all future test certificate results issued by LABOKLIN will only be recorded by the Kennel Club at this time provided they comply with the above protocols.
Please ensure that the veterinary surgeon or veterinary nurse taking the sample complete the vet section on the order form, sign it and stamp it, send it directly to Laboklin and ensure that there stamp is on the package / envelope containing the samples submitted.
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Breeds
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All Dog Breeds
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Russian Black Terrier ( RBT )
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Bulldog
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Dalmatian
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Hungarian Vizsla
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Large Munsterlander
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Spanish Water Dog
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Hungarian Wirehaired Vizsla (Vizslak)
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Kennel Club
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This test is part of the Official UK Kennel Club DNA Testing Scheme in Russian Black Terrier ( RBT ) , Bulldog , Dalmatian , Large Munsterlander , and Hungarian Wirehaired Vizsla (Vizslak).
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The Disease |
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Hyperuricosuria is characterized by elevated levels of uric acid in the urine. This disease predisposes dogs to form stones in their bladders or sometimes kidneys. The trait can occur in any breed but is most commonly found in the Dalmatian, Bulldog and Black Russian Terrier. The mutation was recently described in Spanish Waterdog (https://www.ncbi.nlm.nih.gov/pubmed/26538670). Here at Laboklin we recently tested an Australian Shepherd as carrier of HUU but we have no information about its prevalence in this breed, and therefore testing recomended if your aussie is showing symptoms of the disease.
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Trait of Inheritance |
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Hyperuricosuria is inherited as a simple autosomal recessive trait.
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Inheritance : AUTOSOMAL
RECESSIVE
trait
Sire
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Dam
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Offspring
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clear
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clear
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100% clear
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clear
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carrier
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50% clear + 50%
carriers
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clear
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affected
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100% carriers
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carrier
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clear
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50% clear + 50%
carriers
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carrier
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carrier
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25% clear + 25% affected
+ 50% carriers
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carrier
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affected
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50% carriers + 50%
affected
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affected
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clear
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100% carriers
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affected
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carrier
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50% carriers + 50%
affected
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affected
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affected
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100% affected
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Clear
Genotype: N / N [ Homozygous normal ]
The dog is noncarrier of the mutant gene.
It is very unlikely that the dog will develop Hyperuricosuria / Urate Stones (HUU, SLC). The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.
Carrier
Genotype: N / SLC2 [ Heterozygous ]
The dog carries one copy of the mutant gene and one
copy of the normal gene.
It is very unlikely that the dog will develop Hyperuricosuria / Urate Stones (HUU, SLC) but since it carries the mutant gene, it can pass it on to its offspring with the probability of 50%. Carriers should only be bred to clear dogs. Avoid breeding carrier to carrier because 25% of their offspring is expected to be affected (see table above)
Affected
Genotype: SLC2 / SLC2 [ Homozygous mutant ]
The dog carries two copies of the mutant gene and
therefore it will pass the mutant gene to its entire offspring.
The dog is likely to develop Hyperuricosuria / Urate Stones (HUU, SLC) and will pass the mutant gene to its entire offspring
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Sample Requirements |
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Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs.
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
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4 ) MDR1 Gene Defect / Ivermectin Sensitivity *
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Breeds
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American White Shepherd
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Australian Shepherd
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Bobtail
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Border collie
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Collie
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Elo
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English shepherd
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German Shepherd
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Longhaired Whippet
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McNab Shepherd (McNab Border Collie)
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Old English Sheepdog (Bobtail)
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Rough Collie
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Shetland Sheepdog (Sheltie)
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Silken Windhound
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Smooth Collie
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Waeller (Wäller)
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Kennel Club
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This test is part of the Official UK Kennel Club DNA Testing Scheme in Australian Shepherd , Border collie , Rough Collie , Shetland Sheepdog (Sheltie) , and Smooth Collie.
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The Disease |
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MDR1 is a genetic disorder found in many dog breeds. Affected dogs, when treated with certain common drugs such as Ivermectin and loperamide (Imodium), are unable to pump out these drugs from the brain resulting in poisoning and neurologic symptoms ranging from tremors, anorexia and excess salivation to blindness, coma and even death. Some of these drugs such as Ivermectins, which vets prescribe extensively for the treatment of parasite infections, are able to cause toxicity at 1/200th of the dose required to cause toxicity in healthy dogs.
Scientists discovered that these dogs lack a protein (P-Glycoprotein), which is responsible for pumping out many drugs and toxins from the brain, and that affected dogs show signs of toxicity because they are unable to stop drugs from permeating their brains. Researchers have identified that this condition is due to a mutation in the multi-drug resistance gene [MDR1].
LIST OF DRUGS THAT CAUSE SENSITIVITY TO DOGS WITH MDR1 MUTATION
| Class A |
Do not use these drugs in dogs with MDR1 Gene Defect |
Ivermectine substances "Anti parasites": (Diapec®, Ecomectin®, Equimax®, Eqvalan®, Ivomec®, Noromectin®, Paramectin®, Qualimec®, Sumex®, Virbamec®)
Doramectine substances "Anti parasites": (Dectomax® )
Loperamide substances "ant diarrheal ":
(Imodium®)
Moxidectine substances "Anti Parasites" (Cydectin®, Equest®) |
Class B |
Use only under close control of veterinarian |
Cytostatics "Chemotherapy": (Vinblastine, Vincristine, Doxorubicine, Paclitaxel, Docetaxel, Methotrexat, Vincristine)
Immunosuppressive: (Cyclosporine A)
Heart glycosides: (Digoxine, Methyldigoxine)
Opioids: (Morphium)
Antiarrhythmics: (Verapamil, Diltiazem, Chinidine)
Antiemetics (Ondansetron, Domperidon, Metoclopramide )
Antibiotics (Sparfloxacin, Grepafloxacin, Erythromycin)
Antihistamin (Ebastin)
Glucocorticoid (Dexamethason)
Acepromazine (tranquilizer and pre-anesthetic agent) *
Butorphanol "analgesic and pre-anesthetic agent" *
Other drugs:
Etoposide, Mitoxantrone, Ondansetron, Paclitaxel, Rifampicin |
| Class C |
Can be used only in the permitted application form and dose! |
Selamectin (Stronghold®), Milbemax® and Advocate® . |
* In dogs with the MDR1 mutation, acepromazine and butorphanol tend to cause more profound and prolonged sedation in dogs . It is recommended to reduce the dose by 25% in dogs heterozygous for the MDR1 mutation (MDR1 / N) and by 30-50% in dogs homozygous for the MDR1 mutation (MDR1 / MDR1).
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Trait of Inheritance |
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Dogs that are homozygous for the mutation display, due to a non-functional transporter the ivermectin sensitive phenotype. They can show increased absorption of ivermectin and other substrates e.g. Digoxin, Vincristine, Doxorubicin, Cyclosporin A, Grepafloxacin, Dexamethasone and Loperamide (See list of drugs). Heterozygous animals (carriers) may show sensitivity to avermectins and other drugs. They are able to propagate the responsible mutation throughout the population and it is therefore important that carrier animals are detected prior to breeding.
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Inheritance : AUTOSOMAL
RECESSIVE
trait
Sire
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Dam
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Offspring
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clear
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clear
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100% clear
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clear
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carrier
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50% clear + 50%
carriers
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clear
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affected
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100% carriers
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carrier
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clear
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50% clear + 50%
carriers
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carrier
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carrier
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25% clear + 25% affected
+ 50% carriers
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carrier
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affected
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50% carriers + 50%
affected
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affected
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clear
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100% carriers
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affected
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carrier
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50% carriers + 50%
affected
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affected
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affected
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100% affected
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Clear
Genotype: N / N [ Homozygous normal ]
The dog is noncarrier of the mutant gene.
It is very unlikely that the dog will develop MDR1 Gene Defect / Ivermectin Sensitivity *. The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.
Carrier
Genotype: N / MDR1 [ Heterozygous ]
The dog carries one copy of the mutant gene and one
copy of the normal gene.
The dog may develop MDR1 Gene Defect / Ivermectin Sensitivity.
Since it carries the mutant gene, it can pass it on to its offspring with the probability of 50%.
Affected
Genotype: MDR1 / MDR1 [ Homozygous mutant ]
The dog carries two copies of the mutant gene and
therefore it will pass the mutant gene to its entire offspring.
The dog is likely to develop MDR1 Gene Defect / Ivermectin Sensitivity * and will pass the mutant gene to its entire offspring
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Description |
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This is a mutation-based gene test, which offers many advantages over other methods
The MDR1 gene defect can be detected, using molecular genetic testing techniques. By DNA testing the mutation can be shown directly. The testing is carried out by state of the art laboratory methods and therefore provides a very high accuracy. In general DNA tests can be done at any age. These tests identify both affected and carrier animals. The mutation can be shown directly, what clearly identifies homozygous affected animals. The genetic test offers the unique possibility to identify Ivermectin sensitive animals prior to treatment with Ivermectin and other drugs (see list). * partner lab
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Sample Requirements |
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Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs.
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
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5 ) Progressive Retinal Atrophy (rcd2-PRA) Option 1 by Laboklin
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Breeds
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Collie
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Rough Collie
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Smooth Collie
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Kennel Club
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This test is part of the Official UK Kennel Club DNA Testing Scheme in Rough Collie.
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The Disease |
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Progressive retinal atrophy (PRA) is a leading hereditary cause of blindness in pedigree dogs as is its counterpart retinitis pigmentosa (RP) in humans. PRA shows genetic heterogeneity, as does RP, with several distinct forms already recognized and several more remaining to be investigated.
The retina is a thin layer of neural cells that lines the back of the eyeball. The vertebrate retina contains photoreceptor cells (rods and cones) that respond to light. The cones mediate high-resolution vision and colour vision. The rods mediate lower-resolution, black-and-white, night vision. The degeneration of the retina results in loss of vision, often leading to blindness. One can distinguish between late onset forms of PRA and early onset (whelp-age) dysplastic changes. The clinical and ophthalmologic signs of both forms are similar.
Affected dogs suffer from bilateral Mydriasis, the reflection of the Tapetum lucidum is increased and the retinal vascular network appears atrophic. Currently, there is no treatment for the disease.
Collie:
The “Collie-PRA”, also termed rod-cone dysplasia type 2 (rcd 2), is one form of progressive retina degeneration which is known for a long time as major health problem in the collie breed.
An abnormal development of the cones and rods of the retina leads to night blindness with early onset. First symptoms appear around whelp-age of about 6 weeks. In the majority of cases, a complete loss of vision occur by the age of 1 in rcd2-affected dogs.
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Trait of Inheritance |
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Inheritance : AUTOSOMAL
RECESSIVE
trait
Sire
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Dam
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Offspring
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clear
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clear
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100% clear
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clear
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carrier
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50% clear + 50%
carriers
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clear
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affected
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100% carriers
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carrier
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clear
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50% clear + 50%
carriers
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carrier
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carrier
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25% clear + 25% affected
+ 50% carriers
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carrier
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affected
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50% carriers + 50%
affected
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affected
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clear
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100% carriers
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affected
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carrier
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50% carriers + 50%
affected
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affected
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affected
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100% affected
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Clear
Genotype: N / N [ Homozygous normal ]
The dog is noncarrier of the mutant gene.
It is very unlikely that the dog will develop Progressive Retinal Atrophy (rcd2-PRA) Option 1 by Laboklin. The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.
Carrier
Genotype: N / PRA [ Heterozygous ]
The dog carries one copy of the mutant gene and one
copy of the normal gene.
It is very unlikely that the dog will develop Progressive Retinal Atrophy (rcd2-PRA) Option 1 by Laboklin but since it carries the mutant gene, it can pass it on to its offspring with the probability of 50%. Carriers should only be bred to clear dogs. Avoid breeding carrier to carrier because 25% of their offspring is expected to be affected (see table above)
Affected
Genotype: PRA / PRA [ Homozygous mutant ]
The dog carries two copies of the mutant gene and
therefore it will pass the mutant gene to its entire offspring.
The dog is likely to develop Progressive Retinal Atrophy (rcd2-PRA) Option 1 by Laboklin and will pass the mutant gene to its entire offspring
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Sample Requirements |
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Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs.
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
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Price
for the above 5 tests
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£ 156.00 (including VAT)
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| To order:
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Download
Order Form from this link 
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Complete the order form and send it together
with your samples to the following address:
Laboklin (UK), 125 Northenden Road, Manchester, M33 3HF
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