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Pug Special Offer: DM Exon2 + MH + PDE / NME + PK + PLL
Test number: 8623
Price: £ 144.00 (including VAT) for all 5 tests
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1 ) Degenerative Myelopathy / Degenerative Radiculomyelopathy) DM (Exon 2) / SOD1
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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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Cavalier King Charles Spaniel
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Canaan Dog
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Welsh Corgi (Cardigan)
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Chesapeake Bay Retriever
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Cockapoo (English)
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Cockapoo (American)
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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 ( GIT )
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Golden Retriever
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Goldendoodle
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Pyrenean Mountain Dog (Great Pyrenees)
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Hovawart
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Pumi ( Hungarian Pumi / Pumik )
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Jack Russell Terrier
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Kerry Blue Terrier
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Labradoodle
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Labrador Retriever
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Lakeland Terrier
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Northern Inuit (Tamaskan / British Timber Dog)
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Nova Scotia Duck tolling Retriever ( NSDTR / Toller)
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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 / Toller), Rough Collie, and Smooth Collie.
for UK registered dogs, Laboklin can send results of the tests which are part of the Official UK Kennel Club DNA testing scheme to the Kennel Club (KC) to be recorded and published
as part of the Kennel Club scheme. Results will only be recorded and published by the KC if the result report includes the dog’s
microchip or tattoo number along with either the dog’s registered name or registered number. Any test results that do not carry these identifying
features will not be recorded by the Kennel Club.
In order to ensure that test results are sent to the Kennel Club, customers must also sign the declaration section on the order form to give Laboklin permission to do so.
important:
When you sign the declaration, Laboklin will send the results to the KC on your behalf, and you do not need to send them to the KC yourself again to avoid unnecessary duplications.
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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 |
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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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2 ) MH (Malignant Hyperthermia)
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The Disease |
Malignant hyperthermia (MH) is an inherited disorder of Malignant hyperthermia (MH) is a pharmacogenetic disorder that manifests upon exposure to volatile anesthetics and depolarizing muscle relaxants.
It is characterized by hypercarbia, rhabdomyolysis, generalized skeletal muscle contracture, cardiac dysrhythmia, and renal failure, which develop on exposure to succinylcholine or volatile anesthetic agents. Symptoms of malignant hyperthermia (MH) in dogs include tachycardia, hyperthermia, elevated carbon dioxide production, and can lead to death if the anesthetic is not discontinued.
The canine syndrome can be treated with specific interventions, such as the use of the calcium release channel antagonist dantrolene, which has been shown to be effective in reversing signs of MH. In most reports of MH in dogs, metabolic acidosis is moderate and muscle rigidity is minimal, in contrast to the severity of both in the swine or human condition. |
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Trait of Inheritance |
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Maligant hyperthermia is transmitted as an autosomal dominant trait. This means that a dog can be genetically clear (also called homozygous normal), heterozygous affected (carries one copy of the defective gene) or homozygous affected (carries two copies of the defective gene) concerning MH. Reliable information of dogs that do not carry disease genes is the key to controlling this disease.
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Inheritance : AUTOSOMAL
DOMINANT
trait
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3 ) Pug Dog Encephalitis (PDE) / Necrotizing Meningoencephalitis (NME)
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Kennel Club
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This test is part of the Official UK Kennel Club DNA Testing Scheme in Pug.
for UK registered dogs, Laboklin can send results of the tests which are part of the Official UK Kennel Club DNA testing scheme to the Kennel Club (KC) to be recorded and published
as part of the Kennel Club scheme. Results will only be recorded and published by the KC if the result report includes the dog’s
microchip or tattoo number along with either the dog’s registered name or registered number. Any test results that do not carry these identifying
features will not be recorded by the Kennel Club.
In order to ensure that test results are sent to the Kennel Club, customers must also sign the declaration section on the order form to give Laboklin permission to do so.
important:
When you sign the declaration, Laboklin will send the results to the KC on your behalf, and you do not need to send them to the KC yourself again to avoid unnecessary duplications.
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The Disease |
Pug dog encephalitis (PDE) also know as necrotizing meningoencephalitis (NME), is an inflammatory disorder of the central nervous system that is usually progressive and fatal, it is most commonly found in small dog breeds. Clinical Symptoms include seizures, depression, ataxia, abnormal gait and blindness.
PDE is an auto-immune disease which affects the
central nervous system. |
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Clinical Signs |
First symptoms usually appear at the age of six months to three years and include
disorientation, instability and seizures. Affected dogs hold their head tilted to one side
or shake their heads, they wobble, show an unsteady gait, stumble and fall. Some
walk in circles without being able to stop or scratch the head in an attempt to release
pressure and pain. Evenetually dementia and coma occur. Dogs with encephalitis die 3-6
months after the onset of symptoms. |
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Trait of Inheritance |
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the test result can be either N/N (Clear or non-carrier), N/PDE (Carrier of the mutation) or PDE/PDE (homozygous for the mutation) , however, this is not a diagnostic tests, it is a risk factor mutation, which means that dogs tested affected (PDE/PDE) for the mutation have a higher risk of developing the disease although they may not develop the disease. Clear and carrier dogs have lower risk.
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Inheritance : AUTOSOMAL
trait
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4 ) PK Deficiency (Pyruvate Kinase Deficiency)
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Breeds
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Basenji
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Beagle
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Cairn Terrier
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Labrador Retriever
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Pug
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West Highland White Terrier
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The Disease |
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Pyruvate kinase (PK) is an enzyme critical to the anaerobic glycolytic pathway of energy production in the erythrocyte. If erythrocytes are deficient in PK they are unable to sustain normal cell metabolism and hence are destroyed prematurely. This deficiency manifests as an hemolytic anemia of variable severity with a strong regenerative response. In dogs, the anemia is always severe (PCV 10-20%) whereas in cats the anemia shows a regenerative response. Also associated with the disease in dogs but not cats is a progressive myelofibrosis and osteosclerosis of unknown etiology and this feature, along with liver failure, is the major cause of death in affected dogs.
The life expectancy of affected dogs is shortened and most die before 4 years of age.
PK deficiency has been recognized in both dogs and cats. The dog breeds involved are the Basenji, Beagle, Dachshund, Eskimo, West Highland White Terriers and the Beagle. In cats, PK deficiency has been described in Abyssinian and Somali cats, as well as DSH cats. The feline disease differs from the canine disease in that affected cats can have a normal life span, only intermittently have anemia, and do not seem to develop either osteosclerosis or liver failure. In all breeds the disease is inherited as an autosomal recessive condition. Heterozygotes (carriers) do not have any clinical signs of disease and lead normal lives. They are able to propagate mutations throughout the population however and it is therefore important that carrier animals be detected prior to breeding.
PK deficiency can be detected, using molecular genetic testing techniques, in the Basenji, Beagle, Pug, Labrador Retriever, West Highland White and Cairn Terriers and the Beagle. These tests identify both affected and carrier animals. It is also possible to identify animals deficient in PK activity through enzyme analysis in those breeds where a molecular genetic test is not available.
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Clinical Signs |
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The clinical signs of disease reflect the anemic status of the animal and include exercise intolerance, weakness, heart murmur and splenomegaly. The anemia is macrocytic, hypochromic and highly regenerative in dogs. Radiographs reveal generalized abnormalities in bone density including intramedullary mineralisation of the long bones suggestive of progressive osteosclerosis in dogs.
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Trait of Inheritance |
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PK Deficiency is inherited in an 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 PK Deficiency (Pyruvate Kinase Deficiency). The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.
Carrier
Genotype: N / PK [ 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 PK Deficiency (Pyruvate Kinase Deficiency) 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: PK / PK [ 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 PK Deficiency (Pyruvate Kinase Deficiency) and will pass the mutant gene to its entire offspring
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5 ) Primary Lens Luxation (PLL)
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Breeds
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American Eskimo
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American Hairless Terrier
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Australian Cattle Dog
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Chinese Crested
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Danish Swedish Farmdog
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Fox Terrier
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German Hunting Terrier
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Jack Russell Terrier
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Jagd Terrier
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Lakeland Terrier
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Lancashire Heeler
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Lucas Terrier
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Miniature Bull Terrier
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Norfolk Terrier
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Norwich Terrier
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Parson Russell Terrier (PRT)
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Patterdale Terrier
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Pug
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Rat Terrier
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Sealyham Terrier
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Teddy Roosevelt Terrier
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Tenterfield Terrier
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Tibetan Terrier
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Toy Fox Terrier
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Volpino Italiano
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Welsh Terrier
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Westphalia Terrier
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Wire-haired Fox Terrier
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Yorkshire 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 Chinese Crested, Jack Russell Terrier, Lancashire Heeler, Miniature Bull Terrier, Parson Russell Terrier (PRT), Sealyham Terrier, Tibetan Terrier, and Welsh Terrier.
for UK registered dogs, Laboklin can send results of the tests which are part of the Official UK Kennel Club DNA testing scheme to the Kennel Club (KC) to be recorded and published
as part of the Kennel Club scheme. Results will only be recorded and published by the KC if the result report includes the dog’s
microchip or tattoo number along with either the dog’s registered name or registered number. Any test results that do not carry these identifying
features will not be recorded by the Kennel Club.
In order to ensure that test results are sent to the Kennel Club, customers must also sign the declaration section on the order form to give Laboklin permission to do so.
important:
When you sign the declaration, Laboklin will send the results to the KC on your behalf, and you do not need to send them to the KC yourself again to avoid unnecessary duplications.
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The Disease |
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The zonula fibres secure the position of the lens. Dogs affected from PLL have painful glaucomas and blindness due to a dislocation of the lens due to a breakdown or disintegration of the zonula fibres. PLL can be inherited or acquired. Therefore the disease might also affect genetically free dogs. First clinical signs of the inherited form of PLL are detectable at the very young age of 20 months. A complete lens luxation typically occurs at the age of 3 to 8 years.
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Trait of Inheritance |
Recently, Cathryn Mellersh and colleagues (Farias et al., 2010) identified a mutation in the gene ADAMTS17 that is responsible for the development of inherited PLL.
The mode of inheritance of PLL is autosomal recessive. This means that PLL-affected dogs receive one mutated gene (allel) from the mother as well as from the father. Hence, the parents need to carry at least one mutated allel.
In most cases heterozygous carriers are healthy. However, it is estimated that about 2 – 20 % of the carriers will develop PLL. |
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.
A dog like this is healthy and does not carry the mutated allel responsible for PLL disease. Offspring
of this dog will not get the mutated allel.
Carrier
Genotype: N / PLL [ Heterozygous ]
The dog carries one copy of the mutant gene and one
copy of the normal gene.
The dog has one copy of the normal allel and in addition one copy of the mutated allel. Carriers have
a low risk of developing PLL, however they will pass on the mutation to their offspring. In most cases heterozygous carriers are healthy. However, it is estimated that about 2 – 20 % of the carriers will develop PLL
Affected
Genotype: PLL / PLL [ 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 has two copies of the mutated allel. Affected dogs have a high risk of developing PLL during
their lifetime. The mutated allel will be passed to 100% of the offspring. It is recommended to
examine the eyes of genetically affected dogs every 6 months by a specialist in order to detect the
clinical signs of PLL as early as possible.
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Price
for the above 5 tests
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£ 144.00 (including VAT)
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