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Feline Special Offer:
8 cat DNA tests for just £79.95 including VAT
HCM, HCR, GSD4, PKD, PRA, PK-Def., SMA, Blood Groups

new license: Laboklin holds the exclusive license to test for Warmblood Fragile Foal Syndrome (WFFS)- new price is £48.00
new test: Glaucoma and Goniodysgenesis (GGD) in Border Collie
new test: Acral Mutilation Syndrome (AMS) in English Cocker Spaniel, Springer Spaniel and more ...
new test: Lafora Disease (LAF / LD) / Myoclonic Epilepsy in Beagle and Miniature Wire haired Dachshund
new
Kennel Club DNA testing schemes with LABOKLIN:
Primary Open Angle Glaucoma (POAG) in Basset
Dwarfism (Skeletal Dysplasia 2 / SD2 ) in Labrador Retriever


Beagle DNA Bundle : IGS + Factor VII + MLS + NCCD + Osteogenesis imperfecta + PK + POAG

Test number: 8620

1 ) Cobalamin Malabsorption (Imerslund-Gräsbeck syndrome (IGS))
Breeds
Beagle , Border collie .
Kennel Club
This test is part of the Official UK Kennel Club DNA Testing Scheme in Beagle , and Border collie.
The Disease
Cobalamin malabsorption (merslunf-Gräsbeck Syndrome (IGS)) refers to a genetic disorder by which the vitamin B12, also known as cobalamin, fails to be absorbed from the intestine. Lack of cobalamin leads to changes in the hematopoietic system and to neurological symptoms due to irreversible damage of the brain and nervous system. Symptoms include anorexia, lethargy and failure to gain weight. Cobalamin malabsorption can be managed by supplementation with regular doses of cobalamin.
Trait of Inheritance
recessive trait of inheritance

Inheritance : AUTOSOMAL RECESSIVE trait


 

Sire

 

Dam

 

Offspring

         
clear
clear
100% clear
         
clear
carrier
50%  clear + 50% carriers
         
clear
affected
100% carriers
         
carrier
clear
50%  clear + 50% carriers
         
carrier
carrier
25% clear + 25% affected + 50% carriers
         
carrier
affected
50% carriers + 50% affected
         
affected
clear
100%  carriers
         
affected
carrier
50% carriers + 50% affected
         
affected
affected
100% affected

 


Clear

Genotype: N / N [ Homozygous normal ]

The dog is noncarrier of the mutant gene.

It is very unlikely that the dog will develop Cobalamin Malabsorption (Imerslund-Gräsbeck syndrome (IGS)). The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / IGS [ 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 Cobalamin Malabsorption (Imerslund-Gräsbeck syndrome (IGS)) 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: IGS / IGS [ 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 Cobalamin Malabsorption (Imerslund-Gräsbeck syndrome (IGS)) and will pass the mutant gene to its entire offspring
Sample Requirements
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs. Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
Turnaround
1 - 2 weeks
2 ) Musladin-Lueke syndrome (MLS)
Breed
Beagle .
Kennel Club
This test is part of the Official UK Kennel Club DNA Testing Scheme in Beagle.
The Disease
Musladin-Lueke Syndrome (MLS) manifests with extensive fibrosis of the skin and joints. As puppies, affected dogs fail to thrive. By one year of age the disease stabilizes whereby arthrosis, stiffness, short outer digits as well as a typical flat head shape with higher ear set and slanted eyes are characteristic for this disease. Affected dogs walk upright on their front feeT in what resembles a ballerina stance. Additionally, they show a “happy” temperament.
Trait of Inheritance
Autosomal recessive

Inheritance : AUTOSOMAL RECESSIVE trait


 

Sire

 

Dam

 

Offspring

         
clear
clear
100% clear
         
clear
carrier
50%  clear + 50% carriers
         
clear
affected
100% carriers
         
carrier
clear
50%  clear + 50% carriers
         
carrier
carrier
25% clear + 25% affected + 50% carriers
         
carrier
affected
50% carriers + 50% affected
         
affected
clear
100%  carriers
         
affected
carrier
50% carriers + 50% affected
         
affected
affected
100% affected

 


Clear

Genotype: N / N [ Homozygous normal ]

The dog is noncarrier of the mutant gene.

It is very unlikely that the dog will develop Musladin-Lueke syndrome (MLS). The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / MLS [ 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 Musladin-Lueke syndrome (MLS) 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: MLS / MLS [ 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 Musladin-Lueke syndrome (MLS) and will pass the mutant gene to its entire offspring
Sample Requirements
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs. Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
Turnaround
1 - 2 weeks
3 ) Neonatal Cortical Cerebellar Abiotrophy (NCCD)
Breeds
Beagle , Hungarian Vizsla .
Kennel Club
This test is part of the Official UK Kennel Club DNA Testing Scheme in Beagle.
The Disease
Cerebellar abiotrophy in Beagle is a genetic disease that causes programmed cell-death of Purkinje-cells in the cerebellum. This loss of brain tissue leads to dysfunction of balance and motor funktion. Affected dogs exhibit symptoms soon after birth or in very early age. These include tremor, ataxia and spastic paralysis.
Trait of Inheritance
Autosomal recessive

Inheritance : AUTOSOMAL RECESSIVE trait


 

Sire

 

Dam

 

Offspring

         
clear
clear
100% clear
         
clear
carrier
50%  clear + 50% carriers
         
clear
affected
100% carriers
         
carrier
clear
50%  clear + 50% carriers
         
carrier
carrier
25% clear + 25% affected + 50% carriers
         
carrier
affected
50% carriers + 50% affected
         
affected
clear
100%  carriers
         
affected
carrier
50% carriers + 50% affected
         
affected
affected
100% affected

 


Clear

Genotype: N / N [ Homozygous normal ]

The dog is noncarrier of the mutant gene.

It is very unlikely that the dog will develop Neonatal Cortical Cerebellar Abiotrophy (NCCD). The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / NCCD [ 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 Neonatal Cortical Cerebellar Abiotrophy (NCCD) 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: NCCD / NCCD [ 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 Neonatal Cortical Cerebellar Abiotrophy (NCCD) and will pass the mutant gene to its entire offspring
Sample Requirements
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs. Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
Turnaround
2 - 3 weeks
4 ) Brittle Bone Disease (Osteogenesis Imperfecta)
Breeds
Beagle , Golden Retriever , Miniature Wire haired Dachshund , Miniature Smooth Haired Dachshund , Standard Smooth Haired Dachshund , Standard Wirehaired Dachshund .
The Disease
Osteogenesis Imperfecta is a generalized, inherited bone defect characterized by extreme fragility of bones and loose joints. The bones can break easily, sometimes they break for no known reason. The long bones are slender and have thin cortices. Calluses and recent fractures may be present. The disease can also cause weak muscles, brittle teeth, curved spine and hearing loss. The cause of the disease is a gene defect that affects how the body makes collagen, a protein that helps make bones strong
Clinical Signs
Clinical signs include pain, spontaneous bone and teeth fractures, loose joints, and reduced bone density on radiography. Primary teeth are extremely thin-walled and brittle Osteogenesis imperfecta can range from mild to severe and symptoms vary from one dog to another.
Trait of Inheritance
Osteogenesis imperfecta Is inherited as a autosomal recessive trait

Inheritance : AUTOSOMAL RECESSIVE trait


 

Sire

 

Dam

 

Offspring

         
clear
clear
100% clear
         
clear
carrier
50%  clear + 50% carriers
         
clear
affected
100% carriers
         
carrier
clear
50%  clear + 50% carriers
         
carrier
carrier
25% clear + 25% affected + 50% carriers
         
carrier
affected
50% carriers + 50% affected
         
affected
clear
100%  carriers
         
affected
carrier
50% carriers + 50% affected
         
affected
affected
100% affected

 


Clear

Genotype: N / N [ Homozygous normal ]

The dog is noncarrier of the mutant gene.

It is very unlikely that the dog will develop Brittle Bone Disease (Osteogenesis Imperfecta). The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / OI [ 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 Brittle Bone Disease (Osteogenesis Imperfecta) 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: OI / OI [ 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 Brittle Bone Disease (Osteogenesis Imperfecta) and will pass the mutant gene to its entire offspring
 
Further reading
Further readingHTML file
Sample Requirements
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs. Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
Turnaround
2 - 3 weeks
5 ) PK Deficiency (Pyruvate Kinase Deficiency)
Breeds
Basenji , Beagle , Cairn Terrier , Labrador Retriever , Pug , West Highland White Terrier .
The Disease
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, Dachshund, Eskimo, 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.
Clinical Signs
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.
Trait of Inheritance
PK Deficiency is inherited in an autosomal recessive trait.

Inheritance : AUTOSOMAL RECESSIVE trait


 

Sire

 

Dam

 

Offspring

         
clear
clear
100% clear
         
clear
carrier
50%  clear + 50% carriers
         
clear
affected
100% carriers
         
carrier
clear
50%  clear + 50% carriers
         
carrier
carrier
25% clear + 25% affected + 50% carriers
         
carrier
affected
50% carriers + 50% affected
         
affected
clear
100%  carriers
         
affected
carrier
50% carriers + 50% affected
         
affected
affected
100% affected

 


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
Sample Requirements
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs. Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
Turnaround
2 - 3 weeks
6 ) Primary Open Angle Glaucoma (POAG)
Breeds
Basset , Basset Fauve de Bretagne (Petit) , Beagle , Norwegian Elkhound .
Kennel Club
This test is part of the Official UK Kennel Club DNA Testing Scheme in Basset.
The Disease
A primary open angle glaucoma is a genetic dysfunction of the connective tissue in the eye. Thereby, the aqueous fluid is blocked and the pressure of the eyeball rises. Ultimately, the optic nerve and the retina are damaged leading from partial to complete blindness.

Symptoms include widened pupils, red eyeballs, cloudy cornea and increased eye pressure. Raising eye-pressure causes pain, which leads to the dog loses it's appetite, scratches the eyes, rubbing it's head on walls and exhibit aggressive behaviour.

Early diagnosis allows treatment in decreasing the eye-pressure constantly and thereby preventing damage on the optic nerve and retina.

Trait of Inheritance
Autosomal recessive

Inheritance : AUTOSOMAL RECESSIVE trait


 

Sire

 

Dam

 

Offspring

         
clear
clear
100% clear
         
clear
carrier
50%  clear + 50% carriers
         
clear
affected
100% carriers
         
carrier
clear
50%  clear + 50% carriers
         
carrier
carrier
25% clear + 25% affected + 50% carriers
         
carrier
affected
50% carriers + 50% affected
         
affected
clear
100%  carriers
         
affected
carrier
50% carriers + 50% affected
         
affected
affected
100% affected

 


Clear

Genotype: N / N [ Homozygous normal ]

The dog is noncarrier of the mutant gene.

It is very unlikely that the dog will develop Primary Open Angle Glaucoma (POAG). The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / POAG [ 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 Primary Open Angle Glaucoma (POAG) 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: POAG / POAG [ 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 Primary Open Angle Glaucoma (POAG) and will pass the mutant gene to its entire offspring
Sample Requirements
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs. Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
Turnaround
2 - 3 weeks
7 ) Factor VII Deficiency
Breeds
Airedale Terrier , Alaskan Klee Kai , Beagle , Finnish Hound , Giant Schnauzer , Scottish Deerhound , Welsh Springer Spaniel .
Kennel Club
This test is part of the Official UK Kennel Club DNA Testing Scheme in Beagle.
The Disease
Factor VII deficiency is a mild bleeding disorder caused by lack of factor VII (proconvertin) which plays a role in the blood clotting system. Affected dogs bruise easily and nosebleeds maybe seen. There is often prolonged bleeding after surgery or trauma and, in the cases of major surgical procedures or trauma, bleeding maybe severe.

The condition may go unnoticed for long time and discovered only when a surgery is performed or if the dog had an accident, in both cases increased bleeding will be noticed which can be difficult to control. Your vet will suspect a bleeding disorder.

Trait of Inheritance
Factor V Deficiency follows an autosomal recessive mode of inheritance.

Inheritance : AUTOSOMAL RECESSIVE trait


 

Sire

 

Dam

 

Offspring

         
clear
clear
100% clear
         
clear
carrier
50%  clear + 50% carriers
         
clear
affected
100% carriers
         
carrier
clear
50%  clear + 50% carriers
         
carrier
carrier
25% clear + 25% affected + 50% carriers
         
carrier
affected
50% carriers + 50% affected
         
affected
clear
100%  carriers
         
affected
carrier
50% carriers + 50% affected
         
affected
affected
100% affected

 


Clear

Genotype: N / N [ Homozygous normal ]

The dog is noncarrier of the mutant gene.

It is very unlikely that the dog will develop Factor VII Deficiency. The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / FVII [ 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 Factor VII 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: FVII / FVII [ 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 Factor VII Deficiency and will pass the mutant gene to its entire offspring
Description

Recently, the mutation responsible for this condition has been identified by Dr Urs Giger and researchers at the University of Pennsylvania. The test is now available at LABOKLIN. Factor VII deficiency follows a recessive trait of inheritance, the test identify a dog as affected (2 copies of the abnormal gene), clear (0 copies of the abnormal gene) or carrier (1 copy of the abnormal gene). Only affected dogs with two copies of the affected gene will develop the disease. Since this is am autosomal recessive condition, carrier dogs will not develop the disease but will pass the mutation to their offspring.

Sample Requirements
Whole blood in EDTA tube (0.5 - 1 ml) or Buccal Swabs. Whole blood in EDTA tube (0.5 - 1 ml) or Buccal swabs. .
Turnaround
2 - 3 weeks
Price for the above 7 tests
£ 138.00 (including VAT)

To order:

  • Download Order Form from this link pdf

  • Complete the order form and send it together with your samples to the following address:

    Laboklin (UK),   125 Northenden Road, Manchester, M33 3HF

See Also:
Copper Toxicosis (Copper Storage Disease )  
Progressive Retinal Atrophy (Dominant PRA)  
Globoid Cell Leukodystrophy (Krabbe Disease)  
CSNB (Congenital Stationary Night Blindness)  
CLAD (Canine Leukocyte Adhesion Deficiency)  
Cystinuria  
von Willebrand disease Type II (vWD II)  
PK Deficiency (Pyruvate Kinase Deficiency)  
Fucosidosis  
PFK Deficiency (Phosphofructokinase deficiency)  
Myotonia Congenita  
MH (Malignant Hyperthermia)  
X-Linked Severe Combined Immunodeficiency (X-SCID)  
GM1-Gangliosidosis  
Narcolepsy  
Muscular Dystrophy (MD)  
MPS ( Mucopolysaccharidosis type VII)  
Hereditary Myopathy / Centronuclear Myopathy (HMLR, CNM)  
Canine Cyclic Neutropenia (Gray Collie Syndrome)  
Progressive Retinal Atrophy (cord1- PRA)not recommended for diagnosis  
L-2-HGA ( L- 2 - hydroxyglutaric aciduria )  
von Willebrand disease Type I (vWD I)  
von Willebrand disease Type III (vWD III)  
Neuronal Ceroid Lipofuscinosis ( CL / NCL )  
Trapped Neutrophil Syndrome ( TNS )  
Progressive Red2tinal Atrophy (crd PRA)  
PDP 1 Deficiency (Pyruvate Dehydrogenase Phosphatase 1 Deficiency)  
Factor VII Deficiency  
Progressive Retinal Atrophy (rcd1 PRA)  
Progressive Retinal Atrophy (rcd1a PRA)  
MDR1 Gene Defect / Ivermectin Sensitivity *  
Exercise Induced Collapse ( EIC )  
Dwarfism (Pituitary Dwarfism / Hypopituitarism)  
Degenerative Myelopathy / Degenerative Radiculomyelopathy) DM (Exon 2)  
Greyhound Neuropathy (Hereditary Neuropathy)  
Brittle Bone Disease (Osteogenesis Imperfecta)  
Glycogen Storage Disease (GSDllla)  
Hereditary Cataract (HSF4)  
Neonatal encephalopathy (NE / NEWS)  
Haemophilia B (factor IX deficiency)  
JEB (Junctional Epidermolysis bullosa)  
Primary Lens Luxation (PLL)  
Brachyury (Bobtail Gene / Short Tail)  
Familial Nephropathy (FN) / Hereditary Nephropathy *  
Startle Disease (SD) / Hyperekplexia  
Familial Nephropathy (FN) / Hereditary Nephropathy  
Myostatin Mutation ("Bully" Whippet)/ Double Muscling  
Hereditary Nephritis / Samoyed Hereditary Glomerulopathy  
Episodic Falling in Cavalier King Charles Spaniel (EF)  
Dry Eye and Curly Coat syndrome (CCS)  
CKCS Pack A: Episodic Falling + Dry Eye Curly Coat syndrome  
Haemophilia A (factor VIII deficiency)  
Congenital Hypothyreosis / hypothyroidism ( CHG )  
Hereditary Nasal Parakeratosis (HNPK)  
Juvenile Epilepsy (JE)  
Musladin-Lueke syndrome (MLS)  
Ichthyosis *  
Neonatal Cortical Cerebellar Abiotrophy (NCCD)  
Dwarfism (Skeletal Dysplasia 2 / SD2 )  
Primary Open Angle Glaucoma (POAG)  
Progressive Retinal Atrophy (generalized PRA)  
Progressive Retinal Atrophy (GR-PRA1)  
Progressive retinal atrophy ( rcd4-PRA) / LOPRA  
Alaskan Malamute Polyneuropathy (AMPN / IPAM / HPAM)  
Pug Dog Encephalitis (PDE) / Necrotizing Meningoencephalitis (NME)  
Polycystic Kidney Disease (PKD)  
Pompe's Disease (Glycogen Storage Disease type II / GSDII)  
Primary ciliary dyskinesia (PCD)  
Protein Losing Nephropathy (PLN)  
Late Onset Ataxia (LOA)  
Cobalamin Malabsorption (Imerslund-Gräsbeck syndrome (IGS))  
Collie Eye Anomaly (CEA) / Choroidal Hypoplasia (CH) Option 2 Optigen*  
Retinal Dysplasia (RD) / Oculo Skeletal Dysplasia (OSD)*  
Spinocerebellar ataxia (SCA)  
Cystinuria (Dominant)  
pap-PRA1 (Progressive Retinal Atrophy)  
Progressive Retinal Atrophy (BAS PRA)  
CMSD (Canine Multiple System Degeneration)  
Hereditary Cataract (HSF4) *  
Special offer 4: Juvenile Epilepsy + Furnishing + LSD  
Progressive Retinal Atrophy (prcd-PRA) Option 2: Optigen (8094X)  
Progressive Retinal Atrophy (prcd-PRA) Option 1: (8094P)  
Thrombopathia (Thrombopathy)  
Digital Hyperkeratosis (DH) (Hereditary Footpad Hyperkeratosis / Corny Feet)  
Degenerative Myelopathy / degenerative radiculomyelopathy) DM (Exon 1)  
Degenerative Myelopathy / degenerative radiculomyelopathy) DM (Exon 1 + Exon 2)  
Ectodermal Dysplasia / Skin Fragility Syndrome (ED / SFS)  
Hypomyelination (Shaking Puppy Syndrome) SPS  
Type A PRA * Optigen)  
JRT and PRT Pack A: Late Onset Ataxia (LOA) + Spinocerebellar Attaxia (SCA)  
JRT and PRT Pack B:Late Onset Ataxia (LOA) + Spinocerebellar Attaxia (SCA) + PLL  
Leonberger Polyneuropathy 1 ( LPN1)  
Adult Onset Neuropathy * (AON)  
Hereditary Ataxia (HA)  
Finnish Hound Ataxia / Cerebellar Ataxia (FHA / CAFH)  
Dandy-Walker-Like Malformation (DWLM)  
Persistent Müllerian duct syndrome (PMDS)  
Cone Degeneration (CD) by OptiGen *  
Fanconi Syndrome (FS)  
Lagotto Storage Disease (LSD)  
Juvenile Laryngeal Paralysis & Polyneuropathy (JLPP)  
Progressive Retinal Atrophy (CNGA1 PRA)  
Achromatopsia (day blindness) / ACHM  
Progressive Retinal Atrophy (GR-PRA2)  
Unspecified test  
Postoperative Hemorrhage (P2Y12 / P2RY12)  
Glanzmann Thrombasthenia (Thrombasthenia, Thrombasthenic thrombopathia, GT)  
Prekallikrein Deficiency (KTK) / Fletcher Factor Deficiency  
C3 Deficiency (Complement Component 3 deficiency)  
Congenital Myasthenic Syndrome (CMS)  
Bardet Biedl Syndrome (BBS)  
GM2 Gangliosidosis Variant 0 (Sandhoff Disease)  
Macrothrombocytopenia ( MTC-D )  
Renal Cystadenocarcinoma and Nodular Dermatofibrosis (RCND)  
Vitamin D-dependent Rickets (HVDRR)  
Amelogenesis Imperfecta (AI) / Familial Enamel Hypoplasia (FEH)  
X-linked Myotubular Myopathy (XLMTM)  
Collie Eye Anomaly (CEA) / Choroidal Hypoplasia (CH) Option 1*  
Macrothrombocytopenia ( MTC- R )  
Muscular Dystrophy (MDL)  
Mucopolysaccharidosis type IIIa (MPS IIIA)  
Neuroaxonal Dystrophy ( NAD )  
Progressive Retinal Atrophy (rcd2-PRA) Option 1 by Laboklin  
Ichthyosis ( Epidermolytic Hyperkeratosis (EHK) )  
May-Hegglin Anomaly (MHA)  
Alaskan Husky Encephalopathy (AHE)  
Cerebral Dysfunction (CDF)  
Dwarfism ( Chondrodysplasia )  
Ichthyosis (Congenital Ichthyosis / Great Dane Ichthyosis)  
Hemorrhagic Diathesis / Bleeding Diathesis (Canine Scott Syndrom)  
Glycogen storage disease type Ia (GSD Ia) / VON Grieke Disease  
Gallbladder Mucoceles  
Primary Hyperoxaluria type I (PH I)  
Hyperuricosuria / Urate Stones (HUU, SLC)  
Severe Combined Immunodeficiency (SCID)  
Leukocyte Adhesion Deficiency type III (LAD III)  
Cleft Lip / Palate and Syndactyly (CLPS)  
Progressive Retinal Atrophy (crd1 PRA)  
Progressive Retinal Atrophy (CRD2 PRA)  
Spondylocostal Dysostosis (Comma Defect)  
Canine Multi-Focal Retinopathy (CMR)  
Craniomandibular Osteopathy (CMO)  
Retinal Dysplasia (RD) / Oculo Skeletal Dysplasia (OSD)*  
Special Offer: DM (Exon 2) + MDR1  
Special Offer Chinese Crested: PLL + prcd PRA Option 1 + rcd3 PRA + DM Exon 2  
Warbung Micro Syndrome 1 (WARBM1)  
Raine Syndrome  
van den Ende-Gupta Syndrom (VDEGS)  
Lundehund-Syndrome ( Lymphagetasia )  
Obesity / Adiposity ( ADI )  
Alexander Disease (AxD) / Leukodystrophy  
Spinal Dysraphism / Neural Tube Defects ( NTD )  
Spongy Degeneration with Cerebellar Ataxia ( SDCA1 )  
XL - PRA (Progressive retinal Atrophy)  
Nemaline Myopathy (NM)  
Poodle DNA Bundle: DM exon2 + rcd4 PRA + NE + prcd-PRA option 1 + vWD1  
Golden Retriever DNA bundle: GR-PRA1 + GR-PRA2 + Ichthyosis + prcd-PRA option 1 + Muscular Dystrophy (MD)  
Pug Special Offer: DM Exon2 + MH + PDE / NME + PK + PLL  
Aussie DNA bundle: CEA option * + DM exon2 + HSF4 + MDR1 + MH + NCL + prcd-PRA Option 1*  
Collie DNA Bundle: CEA Option 1 + DM exon2 + HUU (SLC) + MDR1 + rcd2-PRA  
Border Collie DNA Bundle: CEA Option 1 + IGS + MDR1 + SN + NCL + TNS  
Pack A: CNM + DM exon2 + EIC + HNPK + OSD option 1 + prcd-PRA option 1 + SD2  
Pack B: AxD + Cystinuria + Narcolepsy + Obesity + PK + SLC + XL-MTM  
Ichthyosis  
Catalase Deficiency ( CAT ) / Hypocatalasemia / Acatalasia  
Juvenile Myoclonic Epilepsy ( JME )  
Paroxysmal Dyskinesia ( PxD )  
Spongy Degeneration with Cerebellar Ataxia ( SDCA2 )  
Belgian Shepherd Special Offer : SDCA1 + SDCA2  
Sensory Neuropathy ( SN )  
Acute Respiratory Distress Syndrome ( ARDS )  
POAG / PLL Primary Open Angle Glaucoma (POAG) and Primary Lens Luxation (PLL)  
Shar Pei auto-inflammatory disease (SPAID)  
Dystrophic Epidermolysis Bullosa (DEB)  
Doberman DNA bundle (DM2 + vWDI + Narcolepsy + B Locus + D Locus)  
Landseer DNA bundle (Cystinuria + DM2 + SLC + MD + Thrombopathia)  
Rhodesian Ridgeback DNA Bundle (DM2 + Haemophilia B + SLC + JME + MH)  
Rottweiler DNA bundle ( DM2 , SLC , JLPP , CL1 , XL - MTM )  
Leonberger Polyneuropathy 2 ( LPN2 )  
Hereditary Nasal Parakeratosis (HNPK)  
Subacute Necrotizing Encephalopathy (SNE)  
ISDS Exclusive Border Collie DNA Bundle: CEA 1* + IGS + SN + TNS  
Acral Mutilation Syndrome ( AMS )  
Lafora Disease (LAF / LD) / Myoclonic Epilepsy  
Shetland DNA Bundle: CEA option 1 + DM Exon 2 + SLC (HUU) + MDR1 + CNGA1-PRA  
CKCS Pack B: DM Exon2 + Episodic Falling + DryEye + MD + MTC  
Progressive Retinal Atrophy (rcd3 PRA)  
Old English Sheepdog (Bobtail) DNA bundle: DM Exon2 + EIC + HA + MDR1 + PCD  
German Shepherd and Wolfdog DNA Bundle  
Glaucoma and Goniodysgenesis (GGD)  
Leukoencephalomyelopathy ( LEMP )  

 
 
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