prices in Pound
 
  Home
  News and offers
  Genetic Diseases
Dogs
Cats
Horses
Cattle
Pigs
  Coat Colours / Length
  Identity / Parentage
  Reptiles & Amphibians
  Avian Tests
  Profiles / Screening
  Infectious Diseases
  Organs / Parameters
  Downloads & Order
  Order Online
  About Us
  Crufts & Shows
  Contact Us
  Kennel Club ABS
  facebook
 
  **NEW**



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


Pug Special Offer: DM Exon2 + MH + PDE / NME + PK + PLL

Test number: 8623

1 ) Degenerative Myelopathy / Degenerative Radiculomyelopathy) DM (Exon 2)
Breeds
All Dog Breeds , American Eskimo , Chesapeake Bay Retriever , German Shepherd , Golden Retriever , Labrador Retriever , Nova Scotia Duck tolling Retriever ( NSDTR ) , Poodle , Shetland Sheepdog (Sheltie) , Pembroke Welsh Corgi , Cardigan Welsh Corgi , Rough Collie , Smooth Collie , Bernese Mountain Dog , Airedale Terrier , French Bull Dog , Fox Terrier , Boxer , Rhodesian Ridgeback , Jack Russell Terrier , Kerry Blue Terrier , Wire Fox Terrier , Cavalier King Charles Spaniel , Alaskan Malamute , Pug , Borzoi (Russian Wolfhound) , Hovawart , Soft Coated Wheaten Terrier , Canaan Dog , Pyrenean Mountain Dog (Great Pyrenees) , Lakeland Terrier , Hungarian Pumi , Bloodhound , British Timber Dog , Glen Of Imaal Terrier , Utonagan .
Kennel Club
This test is part of the Official UK Kennel Club DNA Testing Scheme in Chesapeake Bay Retriever , German Shepherd , Nova Scotia Duck tolling Retriever ( NSDTR ) , Rough Collie , Smooth Collie , and French Bull Dog.
The Disease
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.
Clinical Signs
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
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;

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 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
Description

Please note that Exon 2 can be found in all dog breeds, there is another DM mutation in Exon 1 which can only be found in Bernese Mountain Dog, click here for more information.

For bernese Mountain Dog we have a special offer for both Exon 1 and Exon 2 at reduced price, click here for more details.

Sample Requirements
Buccal Swabs or 0.5 - 1 ml blood in EDTA Blood Tube Buccal swabs or 0.5 - 1 ml blood in EDTA Blood Tube .
Turnaround
1 - 2 weeks
2 ) MH (Malignant Hyperthermia)
Breed
All Dog Breeds .
The Disease
Maligant hyperthermia (MH) is an inherited disorder of skeletal muscle characterized by hypercarbia, rhabdomyolysis, generalized skeletal muscle contracture, cardiac dysrhythmia, and renal failure, that develops on exposure to succinylcholine or volatile anesthetic agents. Specific interventions, including use of the calcium release channel antagonist dantrolene, are efficacious in reversing signs of the canine syndrome.
Trait of Inheritance
Maligant hyperthermia is transmitted as an autosomal dominant trait. This means that a dog can be genetically clear (also called homozygous normal), heterozygous (carries one copy of the defective gene) or 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.

Inheritance : AUTOSOMAL DOMINANT trait
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 between affected and clear dogs. 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. Another great advantage of the genetic testing is the risk estimate before a narcosis.

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
3 ) Pug Dog Encephalitis (PDE) / Necrotizing Meningoencephalitis (NME)
Breed
Pug .
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.

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.

Trait of Inheritance
autosomal-recessive with variable penetrance;

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 Pug Dog Encephalitis (PDE) / Necrotizing Meningoencephalitis (NME). The dog will never pass the mutation to its offspring, and therefore it can be bred to any other dog.

 

Carrier

Genotype: N / PDE [ 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 Pug Dog Encephalitis (PDE) / Necrotizing Meningoencephalitis (NME) 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: PDE / PDE [ 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 at higher risk of developing Pug Dog Encephalitis (PDE) / Necrotizing Meningoencephalitis (NME) 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 ) 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
5 ) Primary Lens Luxation (PLL)
Breeds
American Eskimo , Australian cattle dog , Chinese Crested , Fox Terrier , Jack Russell Terrier , Jagd Terrier , Lancashire Healer , Miniature Bull Terrier , Parson Russell Terrier (PRT) , Patterdale Terrier , Rat Terrier , Sealyham Terrier , Tibetan Terrier , Toy Fox Terrier , Volpino Italiano , Welsh Terrier , Yorkshire Terrier , Wire-haired Fox Terrier , German Hunt Terrier , Pug , Tenterfield Terrier , Westphalia Terrier , American Hairless Terrier , Lakeland Terrier , Lucas Terrier , Norfolk Terrier , Norwich Terrier , Teddy Roosevelt Terrier , Danish Swedish Farmdog .
Kennel Club
This test is part of the Official UK Kennel Club DNA Testing Scheme in Chinese Crested , Jack Russell Terrier , Lancashire Healer , Miniature Bull Terrier , Parson Russell Terrier (PRT) , Sealyham Terrier , Tibetan Terrier , and Welsh Terrier.
The Disease
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.
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

 

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.

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.
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
Price for the above 5 tests
£ 156.00 (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)  
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)  
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  
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)  

 
 
Home   |   Genetic Diseases  |   Coat Colours / Length  |   Identity / Parentage  |   Reptiles & Amphibians  |   Avian Tests  |   Profiles / Screening  |   Infectious Diseases  |   Organs / Parameters  |   About us  |   Contact Us
LABOKLIN GmbH & Co. KG
ISO / DIN 17025 Accredited Laboratory
© 2007 Laboklin (UK)
125 Northenden Road, Manchester, M33 3HF
Tel. 0161 282 3066