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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 test: Craniomandibular Osteopathy (CMO) in Cairn Terrier , Scottish Terrier and West Highland White Terrier
new
Kennel Club DNA testing schemes with LABOKLIN:
Hereditary Nasal Parakeratosis (HNPK) in Labrador Retriever
Degenerative Myelopathy DM (Exon 2) in German Shepherd and French Bulldog
Primary Lens Luxation (PLL) in Welsh Terrier


Pack B: AxD + Cystinuria + Narcolepsy + Obesity + PK + SLC + XL-MTM

Test number: 8628

1 ) Alexander Disease (AxD) / Leukodystrophy
Breed
Labrador Retriever .
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 Alexander Disease (AxD) / Leukodystrophy. The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / AxD [ 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 Alexander Disease (AxD) / Leukodystrophy 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: AxD / AxD [ 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 Alexander Disease (AxD) / Leukodystrophy and will pass the mutant gene to its entire offspring
Description

Alexander Disease (AxA) (Fibrinoid Encephalomyelopathy) is a genetic disorder characterised by degeneration of the CNS white matter , a leukodystrophy. Clinical signs includes generalised seizure. This degeneration is a disorder of astrocytes and it is associated with a loss of myelin especially in the cerebral white matter. The disease is also know as Leukodystrophy.

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 ) Cystinuria
Breeds
English Mastiff , Labrador Retriever , Landseer , Newfoundland , French Bull Dog , Bulldog , Mastiff .
Kennel Club
This test is part of the Official UK Kennel Club DNA Testing Scheme in Newfoundland.
The Disease
Cystinuria is an inherited disorder caused by a defective transport of the amino acid cystine in the kidney tubules. Normally, cystine is filtered in the kidney and reabsorbed within the tubules, resulting in little cystine in the urine. Dogs with Cystinuria do not properly reabsorb the cystine (and a few other amino acids) in the kidney tubules, causing the urine to contain abnormally high levels of cystine. Cystine is insoluble in neutral pH or acidic urine, so excess urinary cystine results in the formation of crystals, which in turn can lead to formation of cystine calculi (stones) in the kidney and/or the bladder. Dogs suffering from Cystinuria suffer repeated urinary tract inflammations, and are at risk for urinary blockage, which can, if not treated promptly, lead to kidney failure, bladder rupture, and death. The average age of onset of clinical signs attributable to Cystinuria is about 4.8 years, but in Newfoundlands, signs appear as early as 6 months to 1 year, suggesting that Newfoundlands suffer from a more severe form of the disorder than other breeds.
Treatment of the Disease
Cystinuria in humans and dogs is generally treated with compounds that bind cystine and prevent crystal formation. The two most common drugs of choice are 2-mercaptopropionylglycine (MPG) and D-penicillamine. Little information is available on effective dosages for Newfoundlands, however, at least one study indicated that affected Newfoundlands require higher dosages of MPG than other dogs with Cystinuria. D-penicillamine was found to be of minimal benefit in reducing cystine calculi. This may relate to the fact that Newfoundlands suffer from a more severe form of the disorder than other breeds. Treatment with MPG can, in some cases, result in dissolution of cystine calculi, therefore eliminating the need for surgical removal of the stones. Unfortunately, some Newfoundlands are poorly responsive to medical treatment, suffering from recurring bouts of urinary dysfunction, and, oftentimes, requiring surgery to resolve urinary calculi
Trait of Inheritance
Cystinuria in Newfoundlands and Landseer is an inherited autosomal recessive trait. This means that a dog can be genetically clear (homozygous normal), affected, or a carrier (heterozygous). The carriers can spread the diseased gene in the population. Therefore, reliable information on non-affected dogs is the key to controlling this disease.

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 Cystinuria. The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / CY [ 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 Cystinuria 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: CY / CY [ 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 Cystinuria and will pass the mutant gene to its entire offspring
Description

This is a mutation-based gene test, which offers many advantages over other methods

The genetic defect leading to the disease has been identified. By DNA testing the responsible mutation can be shown directly. This method provides a very high accuracy test and can be done at any age. It offers the possibility to distinguish not only between affected and clear dogs, but also to identify clinically healthy carriers. This is an essential information for controlling the disease in the breed as carriers are able to spread the disease in the population, but can not be identified by means of common laboratory diagnostic. If a particularly valuable dog turns out to be a carrier, it can be bred to a non-affected animal, and non-carrier puppies can be saved for the next round of breeding.

 
Further reading
Canine custinuriaHTML 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
1 - 2 weeks
3 ) Narcolepsy
Breeds
Dachshund , Doberman , Labrador Retriever .
The Disease
Narcolepsy is a disabling sleep disorder affecting humans and animals. The disease is characterized by daytime sleepiness, cataplexy and striking transitions from wakefulness into REM sleep. A mutation in the gene encoding the receptor for hypocretin (orexin) receptor 2 was identified as the cause for canine narcolepsy.
Trait of Inheritance
Narcolepsy is an inherited autosomal recessive trait. This means that a dog can be clear (homozygous normal), affected, or a carrier (heterozygous). The carriers can spread the diseased gene in the population. Therefore, reliable information on non-affected dogs is the key to controlling this disease.

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 Narcolepsy. The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / NARC [ 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 Narcolepsy 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: NARC / NARC [ 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 Narcolepsy and will pass the mutant gene to its entire offspring
Description

This is a mutation-based gene test, which offers many advantages over other methods

The genetic defect leading to the disease has been identified. By DNA testing, the responsible mutation can be shown directly. This method provides a very high accuracy test and can be done at any age. It offers the possibility to distinguish not only between affected and clear dogs, but also to identify clinically healthy carriers. This is an essential information for controlling the disease in the breed, as carriers are able to spread the disease in the population, but can not be identified by means of common laboratory diagnostic.

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 ) Obesity / Adiposity ( ADI )
Breeds
Flatcoated Retriever , Labrador Retriever .
Description

A genetic mutation is respobsible for increased appetite and weight gain in Labrador and Flat-Coated retriever. It is well known that labradors are more motivated by food and are more prone to obesity than other breeds. Researchers at the University of Cambridge found that a deletion in the POMC gene is associated with with Weight, Adiposity, and Food Motivation in Labrador Retrievers, this mutation was also identified in Flat-Coated retrievers and associated with the same symptoms. A DNA test is now available at Laboklin to test for the mutation.

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
5 ) PK Deficiency (Pyruvate Kinase Deficiency)
Breeds
Basenji , Beagle , Cairn Terrier , Labrador Retriever , West Highland White Terrier , Pug .
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 ) Hyperuricosuria / Urate Stones (HUU, SLC)
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.

Breeds
All Dog Breeds , Dalmatian , Large Munsterlander , Spanish Water Dog , Bulldog , Russian Black Terrier ( RBT ) , Hungarian Wirehaired Vizsla (Vizslak) , Hungarian Vizsla .
Kennel Club
This test is part of the Official UK Kennel Club DNA Testing Scheme in Dalmatian , Large Munsterlander , Bulldog , Russian Black Terrier ( RBT ) , and Hungarian Wirehaired Vizsla (Vizslak).
The Disease
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.

Trait of Inheritance
Hyperuricosuria is inherited as a simple 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 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
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
7 ) X-linked Myotubular Myopathy (XLMTM)
Breeds
Labrador Retriever , Rottweiler .
The Disease
Myotubular Myopathy is sex-linked inherited muscle disease that occurs in Labrador Retriever and Rottweiler. Symptoms are similar to Centronuclear Myopathy (CNM) / Hereditary Myopathy.

Affected puppies appear normal at birth but they start showing symptoms between 7 and 19 weeks of age. Symptoms include progressive skeletal muscle atrophy, muscle weakness especially in the hind limbs, small stature compared to unaffected littermates, puppies can walk with short choppy strides, collapsing after few strides, difficulty eating due to weakness in mastication muscles, which may lead to dropped jaws, hoarse bark.

The disease progresses rapidly and puppies become unable to stand or raise their heads by 3-4 weeks after the start of the symptoms.

Affected dogs are usually euthanized between 15-26 weeks of age.

Due to the X Linked recessive mode of inheritance, males can either be clear or affected, where as females can be clear, carriers or affected. Females are rarely affected because affected males are usually euthanized at young age. The disease is primarily found in males. Testing enables breeders to identify clear, carrier and affected dogs and help in reducing the occurrence of the disease.

XLMTM is considered rare and we currently have no information about its prevalence in the UK.

Trait of Inheritance
.

Inheritance : X-LINKED RECESSIVE trait

 

Sire

  Dam   Offspring
        Males   Females
clear
clear
100% clear
 
100% clear
             
clear
carrier
50%  clear + 50% affected
 
50%  clear + 50% carriers
             
clear
affected
100% affected
 
100% carriers
             
affected
clear
100%  clear
 
100%  carriers
             
affected
carrier
50% affected + 50% clear
 
50% affected + 50% carriers
             
affected
affected
100% affected
 
100% affected

 


Male:

Clear

Genotype: N [ normal ]

The dog is noncarrier of the mutant gene.

The dog will never develop X-linked Myotubular Myopathy (XLMTM) and therefore it can be used in breeding and should only be bred to clear females.

 

Affected

Genotype: XLMTM [ mutant ]

 

The dog carries the mutant gene and will pass it its entire female offspring.

The dog will develop X-linked Myotubular Myopathy (XLMTM) and will pass the mutant gene to its entire female offspring

Female:

Clear

Genotype: N / N [ Homozygous normal ]

The dog is noncarrier of the mutant gene.

The dog will never develop X-linked Myotubular Myopathy (XLMTM) and therefore it can be used in breeding and should only be bred to clear females.

 

Carrier

Genotype: N / XLMTM [ Heterozygous ]

The dog carries one copy of the mutant gene and one copy of the normal gene.

The dog will never develop X-linked Myotubular Myopathy (XLMTM) but since it carries the mutant gene, it can pass it on to its offspring.

 

Affected

Genotype: XLMTM / XLMTM [ 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 will develop X-linked Myotubular Myopathy (XLMTM) and will pass the mutant gene to its entire female 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 Retinal Atrophy (crd PRA)  
PDP 1 Deficiency (Pyruvate Dehydrogenase Phosphatase 1 Deficiency)  
Factor VII Deficiency  
Progressive Retinal Atrophy (rcd1 PRA)  
Progressive Retinal Atrophy (rcd3 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)  
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)  
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)  
Late Onset Ataxia (LOA) + Spinocerebellar Attaxia (SCA)  
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)  
Beagle DNA Bundle : IGS + MLS + NCCD + Osteogenesis imperfecta + PK + POAG  
Poodle DNA Bundle: DM exon2 + MH + 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 + MH + NCL + TNS  
Pack A: CNM + DM exon2 + EIC + HNPK + OSD option 1 + prcd-PRA option 1 + SD2  
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 + MH + vWDI + Narcolepsy + 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 , MH , XL - MTM )  
Leonberger Polyneuropathy 2 ( LPN2 )  

 
 
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