CCLRC is comprised of a group of dog enthusiasts who share the joy of ownership (and wet-nose) of what we believe to be the world’s greatest dog breed, the Labrador Retriever. Our club was started in 2004 and we continue to grow in membership and exposure to the public. The CCLRC serves Fresno, Madera, Kings and Tulare Counties, but welcomes members from throughout the state.
Values
CCLRC supports events which educate the public about the multi-purpose Labrador Retriever and permit Labrador owners to experience their versatility, including waterfowl and upland gamebird hunting, assistance/support dog work, tracking, agility and competitive conformation and obedience eventing. The CCLRC’s values include promoting quality breeding of Labrador Retrievers in accordance with the standard of the breed, as approved by the Labrador Retriever Club, Inc. (LRC) and the American Kennel Club (AKC). The breed standard describes both the physical appearance and movement of the Labrador and also its famously congenial temperament. We encourage responsible breeding through our Breeder’s Code of Ethics. We promote responsible ownership practices and strive to reduce the number of Labradors without homes or in shelters. We support the AKC Code of Good Sportsmanship.
Mission Statement
CCLRC promotes the preservation the versatile Labrador Retriever with a sound temperament and excellent health.
Breeders code of ethics
It is the intent of the CCLRC to support breeding programs which promote the quality of the breed. Both the sire and dam should display soundness, natural abilities, tractability and conformation as described in the breed standard.
The CCLRC strongly recommends that its members adhere to the following guidelines.
- Breeding dogs should have earned at least one of the following:
- Two (2) championship points awarded by the American Kennel Club
- An Obedience, Tracking or Agility title awarded by the American Kennel Club
- A Judges’ Award of Merit (JAM) or placement in a Derby, Qualifying or Open stake at a licensed field trial
- One leg of any Hunting Retriever title or successful completion of a LRC approved Working Certificate
- Puppies should not be sold wholesale to retail outlets for resale
- Breeders should assure the general health and soundness of the sire and dam at the time of breeding
- Breeders should guarantee the general health of the puppies at the time of sale
- Breeders should breed bitches no more frequently than excellent kennel management dictates based on health and age
- Breeders should promote the use of “Limited Registration” when selling puppies and encourage neutering of all dogs not specifically retained for breeding purposes, in accordance with the veterinarian caring for the dog.
- Participate in the re-homing of any dogs produced who are in need or unwanted
- Strive to reduce the number of Labrador Retrievers in shelters and support Breed Rescue organizations
- Additionally, breeding dogs paired shall be free of genetic disorders for which mandatory testing is policy (below).
- indicates genetic disease evaluation advised as mandatory by CCLRC;
(BD) indicates tests advised at the breeder’s option. These recommendations may change as genetic knowledge increases.
Defect descriptions compliments of VetGen.
1.Orthopedic
Hip Dysplasia and Elbow Dysplasia
Dysplasia (malformation, incongruity) of the hip or elbow joints results in degenerative joint disease (arthritis). Although no genetic test is available at this time, the disorder is inherited, necessitating phenotypic evaluation by radiographs.
Dogs selected for breeding shall have been certified as clear of hip and elbow dysplasia.
If under two (2) years of age, preliminary radiographs finding them to be unaffected by hip or elbow dysplasia as reported by the Orthopedic Foundation for Animals (OFA). Alternatively, this preliminary unaffected status can be certified in writing by two of either board certified radiologists (ACVR) or board certified orthopedic surgeons ACVS) in writing.
After two (2) years of age, both the sire and dam must be certified as unaffected by hip or elbow dysplasia by the OFA.
(BD)Myotubular Myopathy, X-linked
Evaluation via DNA testing from an approved lab is available.
Myotubular Myopathy, X-linked, is a very rare sex-linked condition with symptoms similar to centronuclear myopathy (CNM). It is found in male Labrador retriever dogs and characterized by progressive skeletal muscle atrophy beginning shortly after birth, causing short strides and slow movement compared to littermates and eventually fatally impairing the dog’s gait. Although the mode of inheritance is recessive, male dogs born from a carrier female require just one copy of the mutation, the other gene linked to the X chromosome from which disease gets its name.
Therefore, the disease is limited primarily to male dogs due to the sex-linked mode of inheritance. Unlike the original CNM mutation which is seen worldwide at a high frequency this disease appears to be very recent in origin and therefore isolated and rare. The only affected animals we know of are from western Canada. Result types: Males- Clear or Affected; Females- Clear, Carrier, Affected.
Members are discouraged from using dogs with other orthopedic disorders suspected to be heritable.
(BD)Osteochondritis dissecans (OCD), patellar luxation, lumbosacral (LS) anomalies).
OCD is a defect in the maturation of cartilage to bone in young dogs; luxating patellas cause stifle pain, and LS anomalies can cause back pain. Although no genetic tests are available at this time, the disorders are inherited, necessitating phenotypic evaluation by radiographs.
(BD)SD2-Skeletal Dysplasia 2-“short legs”
Evaluation via DNA testing from an approved lab is available.
Skeletal dysplasia 2 is a conformation related test based on research done at the University of Bern in Switzerland. The group of European researchers identified a mutation in a collagen gene responsible for a very mild form of dwarfism. This is NOT a test for the more extreme form of dwarfism found in Labrador Retrievers (Oculoskeletal dysplasia). While originally described in Europe, it has been detected in the U.S. population, although too few dogs have been tested to know anything of frequency. This is a recessively inherited condition. Labradors affected (2
copies) with this mutation will have a shoulder height that is on average only about 5 centimeters lower than the breed standard accepts. There is a great deal of overlap between affected animals and “normal” animals that just happen to be small. No other joint or ocular problems seem to be associated with this condition. It is found primarily in working lines. Result Types: Clear, Carrier, Affected.
2.Ocular
Breeding dogs shall be examined annually by a Board Certified Veterinary Ophthalmologist (ACVO) and certified to be currently clear of any visible inherited eye anomalies. Such annual exams screen for disorders for which there is no genetic test available.
Entropion
Juvenile Onset Posterior polar subcapsular cataracts (PPSC)
(BD)Puppies should have eye examinations at 6 to 8 weeks of age, before they are placed with new owners to check for retinal folds and the possibility of oculoskeletal dysplasia.
(M)Late-onset form of progressive retinal atrophy known as rod-cone degeneration (prcd-PRA).
Evaluation via DNA testing from an approved lab is available.
Clearance by parentage (parents both prcd-PRA tested and have 2 normal genes) is acceptable.
This is the most common cause of retinal atrophy in many breeds of dog. It is a later onset disease. Most affected dogs do not show signs of vision loss until after four years of age, although an ophthalmology exam may show earlier indications of disease. The PRCD form of PRA is inherited as a recessive trait, meaning carriers show no signs of the disease. Carriers may be maintained in a breeding program but care should be used to never pair them with another carrier when planning a litter. Result types: clear, carrier, affected.
(BD)Retinal dysplasia/oculoskeletal dysplasia (RD/OSD).
Evaluation via DNA testing from an approved lab is available.
OSD carriers, which inherit one copy of the mutated gene, often have significant retinal dysplasia, although silent carriers without retinal folds are possible too. Some dogs with retinal folds have the benign type and are not susceptible to OSD; however, without genetic testing for OSD, they do not pass an eye examination and are not eligible for CHIC certification. Their status changes if the owner shows test results indicating the dog is not a carrier for the OSD mutation.
(BD)MCD-Macular Corneal Dystrophy
Evaluation via DNA testing from an approved lab is available.
MCD is a relatively rare disease which is inherited as an autosomal recessive trait, meaning that both parents must be at least carriers of the disease to produce an affected offspring. The disease is characterized by a diffuse cloudiness of the cornea as well as an abnormally thin cornea in affected animals. This mutation has only been reported in Labrador Retrievers, but may be applicable to designer breeds containing Labrador. In a UK study, a little over 3% of Labradors were carriers of this disease. Result Types: Clear, Carrier, Affected.
(BD)PRA (cord1/crd4) PRA Cord One Dystrophy and PRA (GR PRA 2)
Evaluation via DNA testing from an approved lab is available.
The PRA associated with the cord1/crd4 mutation is an inherited disease of the eye that affects the cone and rod cells that make up the dog’s retina and often leading to blindness. The age of onset is highly variable but when present is usually detectable by the age of three. Researchers at Animal Health Trust have identified a DNA mutation, designated cord1 that is a major risk factor for development of PRA in Miniature Longhaired Dachshunds, Miniature Smooth Haired Dachshunds and English springer spaniel dogs as well as several other breeds. There is currently no treatment for the disease. The cord1 mutation is incompletely penetrant, which means not all dogs with two copies of the mutation will develop PRA. Result types: clear, carrier, affected.
PRA is a descriptive term encompassing a group of diseases with the shared symptom of retinal degeneration. The GR-PRA 2 test has been licensed from the Animal Health Trust where the primary research was undertaken in conjunction with researchers at the
Uppsala University. These are two distinct tests for separate mutations implicated in PRA. They are not the same as the test available for Golden Retriever progressive rod- cone degeneration (PRCD), which is also a form of PRA. Both the PRA-1 and PRA-2 mutations are recessive. As with the GR-PRA 1 mutation, affected animals will experience loss of peripheral vision and night blindness leading to eventual complete blindness. Symptoms for this form of the disease generally start around 4-5 years of age. Result types: clear, carrier, affected.
Note: The American College of Veterinary Ophthalmologists (ACVO) and Orthopedic Foundation for Animals (OFA) have established of an Eye Certification Registry and Clinical Database for Ophthalmic Diagnoses (formerly CERF). Test results from examinations by board-certified veterinary ophthalmologists will be entered in the registry and become part of the clinical database. Dogs with normal results will receive OFA eye certification numbers valid for one year.
3. Cardiac
Evaluation by echocardiography (ultrasound of the heart) for heritable cardiac abnormalities such as tricuspid valve dysplasia is encouraged. Clearance by auscultation alone (stethoscope) is not an acceptable alternative. Echocardiography should ideally be performed by a board certified veterinary cardiologist (DACVIM cardiology).
Tricuspid Valve Dysplasia is a congenital malformation of the tricuspid valve which varies in severity from mild/asymptomatic to severe causing eventual right sided heart failure.
4.Metabolic
Exercise Induced Collapse (EIC)
Evaluation via DNA testing from an approved lab is available.
Exercise Induced Collapse (EIC) is a recessively inherited condition which results in hind limb weakness after relatively short periods of high intensity exercise. EIC is most well-known from the
Labrador Retriever but has now been identified in a number of other breeds. The genetic test is based on the findings at the University of Minnesota that identified the causative mutation.
(BD)Copper Storage Disease (CT – Copper Toxicosis Labrador Type)
Partial Evaluation via DNA testing from approved laboratories is available.
Copper Toxicosis in the Labrador Retriever manifests itself as an accumulation of copper in the liver of affected animals, sometimes to the point of toxicity. Affected dogs have difficulty excreting copper. It is an uncommon but serious diagnosis, relatively late onset disease (middle aged or older dogs) and can be difficult to diagnose. Confirmation currently is only possible with a surgically obtained liver biopsy, an invasive process, evaluated in a particular way (rhodanine scores) requiring a large piece of tissue
The mutation first identified as associated with copper toxicosis in Labradors was identified by researchers at the University of Utrecht, who proposed the primary cause of copper toxicosis in Labrador Retrievers to be a mutant form of gene ATP7B. The Dutch paper found that dogs that inherit two normal versions of the gene (one from each parent) will have normal levels of copper in their livers. Dogs that inherit one normal copy and one mutant copy may have somewhat elevated levels of copper in their liver, while those that inherit two mutant copies may have the highest levels and be at the highest risk for the disease, although there have been some dogs reported that only had one copy and still had dangerously high copper levels. The second gene the Dutch reported to be involved in the Labrador is a mutated form of ATP7A. This was thought to be a “good” mutation which helps minimize the accumulation of copper in the liver. Since this gene is located on the X chromosome, the mutation is inherited as a sex-linked recessive. Males inherit only a single copy of the gene (either normal or mutant) from their mother, while females inherit two copies, one from the x chromosome of each parent. Therefore, males only need to inherit one copy of the mutant gene to help with their copper levels, while females need to inherit two. This is why females are more commonly diagnosed with the disease than males. Since the frequency of the ATP7B CT mutation was believed to be relatively high, fanciers have advised avoiding pairings that might produce two-copy offspring.
A more recent study from the veterinary school in Michigan (2022) studied statistical associations with the genes ATP7A, ATP7B and appropriate liver biopsies from 90 Labrador Retrievers with banked DNA divided into normal controls, intermediate/ambiguous dogs and affected dogs. The results of this study show that the inheritance of Copper toxicosis/hepatitis in the Labrador is more complicated than previously thought, with several confounding factors. More study is needed. Breeders and pet owners do not want to miss the diagnosis and have a devastating
outcome or breed affected dogs, nor do they want to put an unaffected dog through an invasive diagnostic procedure or remove unaffected dogs from the breeding pool. As dietary copper is believed to have an impact on the progression of the disease; careful consideration of diet should be taken in all Labradors.
(BD)Cystinuria
Evaluation via DNA testing from an approved lab is available.
Cystinuria in dogs is indicated by the presence of cysteine stones in the kidney, bladder or ureter. Failure by the kidneys to reabsorb amino acids results in the formation of cystine crystals and sometimes stones in the urine which can lead to blockage of the urethra. While the disease is not genetically sex-linked, it is diagnosed in male dogs more frequently than females due to anatomical differences. The University of Pennsylvania identified mutations responsible for cystinuria in several breeds. Type I Cystinuria is an autosomal recessive disease thus an animal affected with the disease has inherited one copy of the mutation from each parent. Inheriting only one copy from either parent yields carrier status. The disease is not present but the animal must be bred carefully to prevent creating affected offspring.
(BD)HU-Hyperuricosuria
Evaluation via DNA testing from an approved lab is available.
Inherited hyperuricosuria (HU) causes dogs to produce urine with very high levels of uric acid. This can lead to bladder stones, and less frequently kidney stones. The disease is inherited as an autosomal recessive trait. Research performed at the University of California Davis identified the mutation responsible for the disease. The frequency of this disease is very, very low in the Labrador, but carriers have been detected.
(BD)MTC – Macrothrombocytopenia
Evaluation via DNA testing from an approved lab is available.
Macrothrombocytopenia (MTC) is inherited as an autosomal dominant trait. The name is derived from the words macro (large) and thrombocyte (platelets), cells that assist in the blood clotting function. It is characterized by low platelet values and the presence of some larger than normal platelets in circulation. Unlike acquired macrothrombocytopenia (thrombocytopenias secondary to infectious agents, medications, immune-mediated causes), this form does not respond to
treatment. A mutation in the beta-1 tubulin gene has been identified as the cause in a number of breeds. Result types: Clear, Affected heterozygous (one copy), Affected homozygous (2 copies).
(BD)PK – Pyruvate Kinase Deficiency
Evaluation via DNA testing from an approved lab is available.
Pyruvate kinase (PK) deficiency is an inherited lack of an enzyme (pyruvate kinase) in the red blood cells of an affected animal. This enzyme is required for red blood cells to survive for a normal length of time in the blood of the animal, and when it is missing, the red blood cells break down and are destroyed prematurely. This leads to lifelong anemia in the affected animal. The symptoms of anemia are lack of energy, low exercise tolerance, easy fatigability, and probably reduced fertility. This disease is inherited as an autosomal recessive. This means that affected animals have two doses of the mutant gene. Dogs that have one mutant and one normal gene are called carriers. Carriers are not ill (they do not have anemia), but can produce affected offspring if mated to another carrier. Research from the University of Pennsylvania identified a mutation that causes autosomal recessively inherited pyruvic kinase deficiency in Labradors.
Animals with two copies of the mutation usually exhibit severe recurrent anemia.
5.Neurologic
(BD)Degenerative Myelopathy (DM)
Evaluation via DNA testing from an approved lab is available.
Degenerative myelopathy (DM) is a progressive neurodegenerative disease that occurs in many breeds of dog. Research done at the University of Missouri identified mutations in the SOD1-A gene. To date, the major mutation associated with this disease has been detected in 124 breeds, with a second mutation, SOD1-B limited to the Bernese mountain dog. The test for this second mutation is DM-exon1. The disease is an adult-onset condition that has ALS like symptoms: progressive limb weakness and muscle loss, tremors, difficulty rising, and stumbling. Affected animals develop spinal and hind end problems later in life. It is inherited as a recessive disease based on these mutations, but there is also ongoing work to determine other factors that may play a role in severity and age of onset. The mutant allele has about a 7% frequency in Labrador Retriever.
(BD)CMSs-Congenital myasthenic syndromes
Evaluation via DNA testing from an approved lab is available.
Congenital myasthenic syndromes (CMSs) form a heterogeneous group of very rare genetic diseases characterized by a dysfunction of neuromuscular transmission because of mutations in numerous genes. These neuromuscular disorders are characterized by skeletal muscle weakness and fatigue. CMSs disorders occur usually in animals between 6 to 12 weeks of age and appear to be familial and inherited predominantly in an autosomal recessive manner.
(BD)Centronuclear Myopathy (CNM)
Evaluation via DNA testing from an approved lab is available.
Centronuclear Myopathy (CNM) in Labrador Retrievers is a recessively inherited muscular disease. This disease was previously known as Labrador muscular myopathy. The disease is characterized by early onset muscular problems such as awkward gait, fatigue, and difficulty eating. Affected puppies generally begin displaying these problems within a few months after birth.
(BD)Narcolepsy
Evaluation via DNA testing from an approved lab is available.
Narcolepsy is a neurologic condition inherited as an autosomal recessive trait. The disorder in dogs characterized by episodic brief but sudden daytime sleepiness or losses of consciousness, lasting usually several seconds but sometimes as long as last several minutes. An affected dog will have episodes where it collapses suddenly and goes from wakefulness into rapid eye movement (REM) sleep, sometimes accompanied with twitching and whimpering sounds. This can happen during play, eating or other vigorous activity. Episodes can sometimes be interrupted by petting, loud noises or other external stimuli. The condition is quite rare in Labradors, but when present results in dogs which may exhibit cataplexy when overly excited. Affected animals also tend to sleep significantly more than is normal.
6.Cutaneous
(BD)Hereditary nasal parakeratosis (HNPK)
Evaluation via DNA testing from an approved lab is available.
Hereditary nasal parakeratosis (HNPK) is an inherited autosomal recessive skin disorder found in Labrador retriever dogs that is characterized by a buildup of keratinocytes or hyperkeratosis, thickening and hardening of the skin, causing crusts, fissures and depigmentation of the nasal planum. These symptoms begin to develop around 6 months. A mutation for this hereditary skin disorder has been identified at the University of Bern in Switzerland. The disease is inherited in an autosomal recessive manner.
(M) Dilute color (D Locus)
Evaluation via DNA testing from an approved lab is available.
For many years geneticists and breeders have been aware of several locations on the chromosomes, or loci, which are responsible for the color patterns we see in dogs. As with all genetic traits, every animal inherits one copy of each locus from each of its parents. Each of these loci is responsible for one or more traits either independently, or in conjunction with another locus. All of them act on the pathways that produce the two major pigments, phaeomelanin and eumelanin, or affect the distribution of those pigments. The combined effect of all these loci is the color of the dog. Due to the complex interactions of these genes, it is possible for dogs to carry hidden colors which may appear in their offspring. The D locus is the primary locus associated with diluted pigment, which results in coats that would otherwise be black or brown instead showing up as gray, or blue in the case of black, and pale brown/”silver” in the case of brown.
The melanophilin gene has recently been shown to be responsible, but not all of the dilute causing mutations have been identified yet. The position of CCLRC is that Silver dogs should not be bred, and dogs carrying the dilute gene should not be bred. Screening for the dilute gene before breeding is mandatory to meet our breeder’s code of ethics.
(BD)Coat Length
Evaluation via DNA testing from an approved lab is available.
The length of a dog’s coat is of interest to many. It has recently been demonstrated that in many breeds, the gene FGF5 is responsible for whether a dog has a long coat (rough or fluffy), or a short (smooth) coat. The genetic test detects the presence or absence of the recessive allele that results in long coats when present in two copies, and as such allows dogs with short coats that carry a hidden “long coat” allele to be detected.
Note: The OFA created the Canine Health Information Center (CHIC) by partnering with the LRC to research and maintain information on the health issues prevalent in specific breeds. Dogs tested in accordance with that protocol are recognized with a CHIC number and certification. https://www.ofa.org/about/chic-program and https://www.ofa.org/about/chic-program#brdreqs.html?breed=PM