Dilute Gene (October 22, 2016)|
|*** JUST SAY NO TO "SILVER" LABS|
The American Kennel Club (AKC) (and all other reputable kennel clubs around the world) recognizes three coat colors in the Labrador: black, yellow and chocolate. These colors are inherited based on genes at two loci: B and E. In recent years, other colors have become more prominent in the breed. Breeders refer to these colors as ‘silver’, ‘charcoal’ and ‘champagne’. In order to obtain these new colors, a recessive D locus dilution factor (d) must be introduced into the population. According to literature, the dilution factor was not originally a part of the Labrador Retriever breed, and therefore, controversy surrounds the topic.
Information known about the dilution factor’s lack of presence in the Labrador suggests that it was introduced into the breed in the United States, at some point in time, probably in the late 1940s, early 1950s, by crossbreeding. Research has shown that some dogs with coat color dilution are prone to hair loss and reoccurring skin problems. These conditions should be selected against by eliminating dilution factors within the Labrador population.
The Labrador Retriever breed should be consistent with its breed standard, and dilute colored dogs incorrectly represent the purebred breed.
The Labrador Retriever breed, as it was developed and registered in the United Kingdom, never (until 2006) carried the dilution factor. A survey in the United Kingdom, Europe, Canada and the United States shows that no reputable Labrador breeder has ever had a puppy carrying the dilution factor, so it is hard to explain the direct cause of a mutation in the breed. There is no other explanation than that crossbreeding occurred with a breed carrying dilution, probably the Weimaraner, and they passed the d allele down to offspring.
There are many breeders in the United States who specialize in breeding diluted “Labradors”. Diluted dogs typically have a metallic-looking sheen to the hair. A typical Labrador with a black phenotype can have the genotype: BBEE, BBEe, BbEE or BbEe. A Labrador with a chocolate phenotype will have either the bbEE or the bbEe genotype. A dog displaying a yellow coat must have the homozygous recessive genotype at the E locus, and therefore can be BBee, Bbee or bbee. It is possible for these genotypes to be diluted if the dog carries two copies of the recessive dilute gene, dd. Dogs that carry at least one D will not have a diluted coat. If a dog carries the Dd genotype at the D locus, one copy of the dilute gene is present. If bred to a bitch carrying a dilute gene (Dd or dd), diluted offspring could be produced.
Health problems and misconstruing of breed standards due to dilution
Various expressions of the dilution gene have been noted. Some dogs with dilute color display minimal or no health problems; other dogs experience hair loss and skin problems. Color dilution alopecia (CDA) and black hair follicular dysplasia (BHFD) can accompany coat color dilution. These diseases cause recurrent skin inflammation and drying, bacterial infections of hair follicles and severe hair loss. Late 2013 a 12-week-old female silver Labrador Retriever was submitted to the Comparative Ocular Pathology Laboratory of Wisconsin, and was diagnosed with Malignant Uveal Schwannoma. Scientists believe that the dilute color mutation may contribute to the cause.
Other disorders that could travel with the dilution gene are heritable Weimeraner genetic issues such as trembling disorders, autoimmune related vaccination sensitivity and intolerance, Von Willebrands Disease, hyperuricosuria causing painful bladder and kidney disease, and behavioral problems that are more common in the Weimaraner, such as separation anxiety, and dominant, protective, territorial temperament. Minimizing occurrence of these conditions would mean minimization of the dilute mutation. Selection against dilution is important in breeds that display health issues associated with the mutation. It is also important to minimize the dilution mutation in breeds that do not have a standard written which include these colors. The Labrador Retriever is currently one of these breeds. Dilute colored Labrador retrievers are a disqualification according to breed standards. Those dogs carrying the dilute gene should not be registered as purebred Labrador Retrievers.
The Labrador Retriever Club Inc. is the AKC Parent Club of the Labrador Retriever. On May 12, 2014, the LRC published the following message on their website: “Very exciting news – the OFA has agreed to maintain a database of Labradors who have been permanently identified (microchip or tattoo ) and have been tested for the d gene. Dogs having the genotype dd will be listed as affected, Dd as carriers of the dilute gene and DD as clear of the dilute gene. This is great news for us.”
Note: The Orthopedic Foundations for Animals (OFA) only registers hereditary diseases (or the lack of those) in their databases. So it’s not a simple matter of “a different colour”.
Although findings of these various studies do not definitively explain the cause of dilution in dog coat colors, they help us to understand the correlation between dilution and the MLPH gene. Knowledge that the MLPH gene mutation is responsible for dilution has allowed DNA testing companies to begin testing for the mutant dd allele. These tests can help identify carriers of the d gene, and therefore, can help to eliminate it from populations, such as the Labrador retriever, in which it is undesirable. Responsible breeders should take the time, and spend the money, to have their breeding stock genetically tested at the D locus. Labradors displaying dilution, ‘silver’, ‘champagne’ or ‘charcoal’, coloration (dd) should not be used for breeding. Ideally, only Labradors with genotype DD at the dilution locus should be used for breeding.
Throughout the years, Labrador breeders have worked diligently to eliminate undesired traits and illnesses in the breed. A complete elimination of coat color dilution in the Labrador retriever would take a very long time, through DNA testing and breeding stock selection. Kennel clubs and breed clubs are expected to respect the breed standard and the closed character of the studbooks. No respect of the breed standard and the closed character of the studbooks is shown by the common practice of registering “silver” as chocolate, “charcoal” as black, and “champagne” as yellow. Labrador retriever breeders are equally expected to follow the breed standard as currently written when selecting parents for future litters.
The situation in Europe
The AKC registration of “silver”, “charcoal” and “champagne” dogs as chocolate, black or yellow Labrador Retrievers, without any restrictions, has resulted in the disturbing fact that in 2011 the first American dilutes were imported into the United Kingdom, and that these dilutes were registered by The Kennel Club, also without any restrictions. As a result, hundreds of dilutes were born in the United Kingdom, and most of them were registered by the K.C. as completely normal black, chocolate or yellow Labrador Retrievers. The Kennel Club told the Labrador parent club that “DNA-tests” proved that these dogs were purebred Labrador Retrievers, and that there was nothing they could do about it.
The Kennel Club did not mention when these “tests” took place. However, it’s a matter of fact that these tests are extremely unreliable. Yes, the tests could show that the parents and grandparents of a certain dog are Labrador Retrievers, but does that make a dog a purebred Labrador? Even the most modern and sophisticated tests are not able to say something about anything that happened more than three generations ago, while many dilutes have a history that goes back to the 1970s, or even to the 1950s.
So, instead of using an extremely unreliable test to “prove” that a Labrador is purebred, the K.C.’s should use a test that is reliable: any dog carrying the d-gene can not be a purebred Labrador Retriever and should be excluded from the registry.
The D Locus (Dilute) coat color test reliably determines if a dog has one of the following genotypes at the D locus:
This dog carries two copies of D which does not result in the "dilution" or lightening of the black and yellow/red pigments that produce the dog’s coat color. The base coat color of this dog will be primarily determined by the E, K, A, and B genes. The dog will pass on D to 100% of its offspring.
Interpretation: Non dilute
This dog carries one copy of D and one copy of d which does not result in the "dilution" or lightening of the black and yellow/red pigments that produce the dog’s coat color. The base coat color of this dog will be primarily determined by the E, K, A, and B genes. The dog will pass on D to 50% of its offspring and d to 50% of its offspring.
Interpretation: Non dilute (Carrier)
This dog carries two copies of d which results in the "dilution" or lightening of the black and yellow/red pigments that produce the dog’s coat color. However, this variant modifies or "dilutes" the base coat color of the dog that is primarily determined by the E, K, A, and B genes. The dog will pass on d to 100% of its offspring.
Hereditary Nasal Parakeratosis ( HNPK ) (October 22, 2016)|
|Hereditary nasal parakeratosis (HNPK) is an inherited autosomal recessive disorder in Labrador Retrievers. A mutation T>G in the SUV39H2 gene causes the nose to dry out leading to chronic irritation and inflammation of the noses skin.|
Symptoms of the disorder generally appear around 6 to 12 months of age. Affected dogs develop dry, rough; gray to brown crusts on the surface and edge of the nose. In some cases, painful cracks around and on the tip of the nose develop and if not treated develop superficial bacterial infections. Over time, the nose often begins to depigment changing skin color from dark to light in color. Although the disorder is nonlife threatening, continuous care to reduce the recurrence of excessive nasal crusting is required throughout the life of the dog.
Because HNPK is a recessive disorder, a dog must have two copies of the mutation in order for the disease to manifest. This means that a dog can have one copy of the mutation and not experience any signs or symptoms of HNPK; this dog would be known as a carrier. The carrier can then pass on either the normal gene or the mutated gene to any offspring. If two carriers are bred, there is a 25% chance of haveing a dog that recieves two mutated copies of the gene and would be affected by HNPK.
Progressive Retinal Atrophy (October 22, 2016)|
|**** PRA has been discovered in Labradors as well as NOW Rat Terriers... ****|
The genetic disorder, prcd-PRA , causes cells in the retina at the back of the eye to degenerate and die, even though the cells seem to develop normally early in life. The “rod” cells operate in low light levels and are the first to lose normal function. Night blindness results. Then the “cone” cells gradually lose their normal function in full light situations. Most affected dogs will eventually be blind. Typically, the clinical disease is recognized first in early adolescence or early adulthood. Since age at onset of disease varies among breeds, you should read specific information for your dog. Diagnosis of retinal disease can be difficult. Conditions that seem to be prcd-PRA might instead be another disease and might not be inherited. OptiGen’s genetic test assists in making the diagnosis. It’s important to remember that not all retinal disease is PRA and not all PRA is the prcd form of PRA. Annual eye exams by a veterinary ophthalmologist will build a history of eye health that will help to diagnose disease.
Unfortunately, at this time there is no treatment or cure for PRA. If your dog is affected, you may find it helpful to read about other owners’ experiences living with blind dogs. (suggested links:www.eyevet.org and www.blinddogs.com)
Prcd-PRA is inherited as a recessive trait. This means a disease gene must be inherited from each parent in order to cause disease in an offspring. Parents were either “carrier” or affected. A carrier has one disease gene and one normal gene, and is termed “heterozygous” for the disease. A normal dog has no disease gene and is termed “homozygous normal” – both copies of the gene are the same. And a dog with two disease genes is termed “homozygous affected” – both copies of the gene are abnormal.
It’s been proven that all breeds being tested for prcd-PRA have the same disease caused by the same mutated gene. This is so, even though the disease might develop at different ages or with differing severity from one breed to another.
Although prcd-PRA is inherited, it can be avoided in future generations by testing dogs before breeding. Identification of dogs that do not carry disease genes is the key. These "clear" dogs can be bred to any mate - even to a prcd-affected dog which may be a desirable breeding prospect for other reasons. The chance of producing affected pups from such breedings depends on the certainty of test results. Again, you’ll find the specific information on certainty of test results for your dog by linking to breed specific information.
Though the condition is considered rare,with around 3% of Labs identified as a carriers, is devastating to those whose dogs develop the disease.
Degenerative Myelopathy (October 22, 2016)|
|What is Degenerative Myelopathy?|
Degenerative myelopathy is a progressive disease of the spinal cord in older dogs. The disease has an insidious onset typically between 8 and 14 years of age. It begins with a loss of coordination (ataxia) in the hind limbs. The affected dog will wobble when walking, knuckle over or drag the feet. This can first occur in one hind limb and then affect the other. As the disease progresses, the limbs become weak and the dog begins to buckle and has difficulty standing. The weakness gets progressively worse until the dog is unable to walk. The clinical course can range from 6 months to 1 year before dogs become paraplegic. If signs progress for a longer period of time, loss of urinary and fecal continence may occur and eventually weakness will develop in the front limbs. Another key feature of DM is that it is not a painful disease.
What causes Degenerative Myelopathy?
Degenerative myelopathy begins with the spinal cord in the thoracic (chest) region. If we look under the microscope at that area of the cord from a dog that has died from DM, we see degeneration of the white matter of the spinal cord. The white matter contains fibers that transmit movement commands from the brain to the limbs and sensory information from the limbs to the brain.This degeneration consists of both demyelination (stripping away the insulation of these fibers) and axonal loss (loss of the actual fibers), and interferes with the communication between the brain and limbs. Recent research has identified a mutation in a gene that confers a greatly increased risk of developing the disease.
How do we treat degenerative myelopathy?
There are no treatments that have been clearly shown to stop or slow progression of DM. Although there are a number of approaches that have been tried or recommended on the internet, no scientific evidence exists that they work. The outlook for a dog with DM is still grave. The discovery of a gene that identifies dogs at risk for developing degenerative myelopathy could pave the way for therapeutic trials to prevent the disease from developing. Meanwhile, the quality of life of an affected dog can be improved by measures such as good nursing care, physical rehabilitation, pressure sore prevention, monitoring for urinary infections, and ways to increase mobility through use of harnesses and carts.
Centronuclear Myopathy (January 5, 2014)|
Centronuclear Myopathy (CNM) is a grave disease that has been a major concern in Labrador Retrievers globally since the 1970’s. CNM, was first discovered in 1976.
Puppies with CNM are almost in distinguishable from their littermates at birth. When they are 4 wks old, they lack or show weak tendon reflexes and weigh significantly less than their littermates. Some of these signs could be cause by other diseases and thus are not sufficent for identifying affected puppies.
The disabling condition sets in by the 3 – 5 mns of age when puppies begin to walk with an akward gait and experience decreased exercise tolerance. Cold enviroments worsen their general muscle weakness. Clinical signs are progressive but generally stabilized by around 12-18 mns of age. There is NO recovery of the muscles & no medications help.
Some puppies with CNM are euthanized when signs appear. Others that are mildly affected can live up to about 12 yrs with continual special care and environmental conditions. Weakness in the muscles of the esophagus can cause megaesophagus,a secondary condition that leads to eating problems.Pneumonia due to food particles getting into the lungs is a frequent cause of early death.
When a dog is only a carrier, there are no physical symptoms and the Labrador will live a normal, healthy, CNM free life. The only way a carrier can be detected is if the (#1) The dog is tested or (#2) The Dog has produced a litter that has had an affected pup which also means in fact that both parents are definitely carriers.
It is OK to breed carrier to clear but not carrier to carrier.
A carrier Labrador bred to a clear Labrador will have a litter with carriers, but no affected pups. It takes two carriers bred together to produce a litter with the potential of affected pups. If a dog produces even one affected pup, it is a carrier for sure. The CNM test is a tool that will enable breeders to avoid ever producing an affected pup. (Genetics are not absolute, variances can occur and are based solely on probability. However, following these standards, we can guarantee that there will be no affected puppies produced.)
CNM: IMPLICATIONS FOR BREEDING
(Genetics are not absolute, variances can occur and are based solely on probability. However, following these standards, we can guarantee that there will be no affected puppies produced.)
Clear dogs: no copies of the mutation
CLEAR X CLEAR dog: 100% of pups clear
CLEAR X CARRIER : 50% of pups clear, 50% of pups carriers*
CLEAR X AFFECTED: 100% of pups will be carriers
There is absolutely no reason why you shouldn't breed a "Carrier" to a "Clear". There are many reasons that breeders choose to breed "clears" to "carriers" of this disease but should not be misunderstood. National Field Champion Bloodlines that would simply fade away, are preserved through critically studied genetics and "Bred Out" to ensure that all new puppies are completely clear of this disease.
Excercise Induced Collapse ( EIC ) (February 13, 2013)|
|EIC is a common cause of exercise intolerance and subsequent collapse in what appears to be a healthy adult Labrador Retriever. Dogs with EIC are normal at rest and able to tolerate mild to moderate exercise but occasionally become in coordinated and collapse after 5 to 15 minutes of strenuous exercise. The syndrome of exercise intolerance and collapse (EIC) is being observed with increasing frequency in young adult Labrador Retrievers. Most, but not all, affected dogs have been from field-trial breedings.|
Thirty percent of all tested Labrador Retrievers carry the EIC gene. This is not a problem unless a breeder unknowingly breeds one carrier to another carrier and ends up with affected Labrador Retriever puppies. It can take up to 5 years for symptoms to appear, so it is important that breeders test for this gene. It is also important for buyers to educate themselves and learn about this debilitating problem. Ask your breeder if their dogs have been tested and find a breeder who has done so to prevent problems later on in your dog's life.
Every dog inherits 2 copies of every gene - one from its dam and one from its sire. EIC is inherited as an autosomal recessive trait, which means that all affected dogs (those showing signs of collapse) have 2 copies of the mutated gene - one that they got from their dam and one from their sire.
Clear dogs: These dogs have no copies of the gene, and do not have EIC, nor will they show signs of collapse. If bred, they will not pass a copy of the EIC mutation on to any of their puppies.
Carriers: Have one copy of the mutated gene that they got from either their dam or their sire and they have one normal copy of the gene that they got from the other parent. These dogs do not have EIC and will not show signs of collapse. They will, however, pass their copy of the mutated gene on to approximately half of their puppies.
Affected dogs: have 2 copies of the mutation, one of which came from each parent. Dogs with 2 copies of the mutated gene (affected dogs) have EIC and most will show occasional signs of exercise intolerance or collapse when participating in trigger activities with a very high level of excitement or stress. Some affected dogs will never exhibit signs of EIC - this could be because they do not participate in high excitement strenuous activities or because they have a laid-back temperament. Affected dogs can tolerate mild to moderate exercise, but 5 to 20 minutes of strenuous exercise with excitement induces weakness and then collapse. Severely affected dogs may collapse whenever they are exercised to this extent - other dogs only exhibit collapse sporadically and all of the factors important in inducing an episode have not yet been well established.
A rocking or forced gait is usually the first sign of an oncoming collapse. Many affected dogs will continue to run while dragging their back legs. it is as if the back legs can't hold up your dog's weight. You may just think your Lab is uncoordinated, especially in the hind end. In some dogs the rear limb collapse progresses to forelimb weakness and occasionally to a total inability to move. Complete collapse can occur and your dog may even appear stunned or disoriented. The symptoms can continue to worsen even after exercise is stopped. A few affected dogs have died during exercise or while resting immediately after a collapse of exercise-induced collapse so an affected dog's exercise should ALWAYS be stopped at the first hint of an EIC attack.
Most dogs recover quickly and are usually normal within 5 to 25 minutes with no residual weakness or stiffness. Dogs are not painful during the collapse or after recovery. Massage of the muscles or palpation of the joints or spine is not uncomfortable. Affected dogs are not stiff or sore or limping upon recovery. Body temperature is normal at rest in dogs with EIC but almost always dramatically increases at the time of collapse.
Primary Lens Luxation (September 30, 2010)|
|***Important Information About PLL ***|
Lens Luxation is the dislocation or displacement of the lens within the eye. The lens is the clear structure in the eye,consisting of two rounded or conves surfaces,that focuses light rays to form an image onto the retina. Normally the lens is suspended between the iris ( the colored portion of the eye ) and the vitreous ( the clear gel in the back of the eye ), and is held in place by small fibers called zonules or suspensory ligaments.
Should the zonules break, the lens can either become partially dislocated (subluxated) from it normal position or completely dislocated ( luxation . When the lens detaches and falls forward into the anterior chamber in front of the pupil, it's called anterior luxation. When it falls back into the rear portion of the eye, it is called posterior luxation.
Primary Lens Luxation ( PLL )is an inherited disorder in which the zonuless or the suspensory fibers degenerate. The condition occurs mainly in the Terrier breeds,and sporadically in other breeds.Although the underlying reasons for the lens luxation are not well understood, inflammation or defect in the zonules may play a role. WIth PLL, both eyes are prone to dislocation of the lens. The typical age of onset for PLL is 4 to 8 yrs. A luxated lens will cause pain and inflammation and requires immediate veterinary attention. Expensive surgery is often indicated, and the dog's vision may or may not be able to be saved.
Until October 2009,there was no test available for PLL. The University of Missouri, College of Veterinary Medicine,through the partnership of OFA, now has a DNA test for this mutation.
The DNA test will categorize dogs as:
AFFECTED = Two mutated copies of the gene. At HIGH RISK for lens luxation and should NOT be used for breeding.
CARRIER = One normal and one mutated copy of the gene. At LOW RISK for lens luxation,but could pass either the normal copy or the mutated copy of the gene on its offspring. Carriers can be used for breeding, with caution... the only appropiate mate for carrier is a clear,so as not to produce any affected puppies.
CLEAR = Two normal and one mutated copy of the gene on its offspring. At NO RISK for lens luxation. Can only pass normal copy of the gene on to its offspring.
CLEAR BY PARENTAGE = Both Sire and Dam are clear, and that pair bred together can never produce an affected or a carrier. CLEAR x CLEAR is the ideal breeding pair.
Odds of in heritance for the PLL Gene:
CLEAR X CLEAR = 100% CLEAR
CLEAR X CARRIER = 50% CLEAR/50% CARRIER
CLEAR X AFFECTED = 100% CARRIER
CARRIER X CARRIER = 25% CLEAR/50% CARRIER/25% AFFECTED
CARRIER X AFFECTED = 50% CARRIER/50% AFFECTED
AFFECTED X AFFECTED = 100% AFFECTED
*** NOTE ***
FROM THE OFA!!!!!
FROM CANINE GENETIC DISEASES!!!!!
FROM THE University of Missouri!!!!!
FROM THE ANIMAL HEALTH TRUST!!!!!
Rat Terrier Colors (September 28, 2010)|
|We will displaying as much of the colors with pictures as we are able to. Most of the pictures we are using, in this album are from our own past litters. We will have 3 pics of each puppy 1st as a newborn/1 wk old & the 2nd pic at about 12 wks old & the 3rd pic at 1 yr old. So you can see the colors as they get older...||0 Visits|
THE MERLE GENE (October 9, 2010)|
Ah, the scary Merle Gene "oooooo". Or rather NOT so scary.
Merle is not all that scary. There are a few basic guidlines. Guidlines that govern all the merled breeds.
The #1 guidline is and should always be NO MERLE SHOULD EVER BE BRED TO ANOTHER MERLE. This has been a guidline for many decades in the Aussie ring.
Merle is a dominant gene and has no recessive counterpart. This means that only a merle dog will pass its gene to its offsring. Only the main coat color (Eumelanin) we be affected. The secondary colors (Phaeomelanin) or tans, along with white (absence of Melanin) will not change. However the main color covers the entire dog and is affected by the tan & white markings pushing it out of certain areas. In these areas the merle gene can also reside. It can be hidden by the tan and white and not show anywhere else on the body. We call these dogs Cryptic or Phantom Merles. They are merles that have no visible merling but, will produce merled offspring when bred to known solid mates.
Merle In The Rat Terrier:
In the Rat Terrier this can become slightly more complicated. The Color gene pool becomes larger and more unstable. Do to this a few more guidlines come into play. Being new to the merle Rat Terrier ourselves it has been a learning experiance. We would like to thank a very good friend Rhonda Gregg of RGRats for her guidance. As she recently told us, A merle Rt should only be bred to a foundation/dark color Rt. Meaning the main colors being Black, Chocolate, Blue & Pearle. They can be Bi-color or Tri-color or, even Piebald. But, you should refrain from breeding to any of the Sables or Fawns. The genes known to produce these patterns will also mask the merle gene. A mistake we made this year in our own breedings. Yes I will admit it. "I made a mistake!". As an Aussie breeder and genetics fancier, I could kick my self right in the a&&. But, this is how we learn. How mankind has learned for many millenia.
Merle To Merle? Why Not?
I will tell you why not. Some have done it and done it well. I do not and will not ever say it is ok. Someday I may chance it in my Aussies or may have an oopsie (not likely but, you never know). I will never ever EVER do this in the Rt.
The Rat Terrier has the well known Piebald Pattern. This pattern can and will mask the merle pattern.
Merle to Merle breedings in Aussies have produced White or nearly White pups. This is caused by the merle gene diluting the main color normally, than diluting that again, stripping out all traces of color in the already dilute areas. These pups are known as Double Merles and some times Leathel Whites.
However Leathel White is not a true discription, as it is a horse illness, not known in dogs.
In the Double Merle complication may arise, due to the severe lack of pigment. The DM may be blind, deaf or both. This happens depending on the location of the white areas. Ex. White haired, pink skinned ears could indicate deafness or White hair, pink skin around the eyes could indicate blindness. Also it has been my knowlage that a DM with a mostly white body could be sterile or have other issues.
And here's the question, plain and simple. If you breed two merle Rt together. How will you know if the white or nearly white puppy is a Piebald or a Double Merle?????? I say just don't chance it. I know i wont.
Now Again: How About Merle To Sable or Fawn?
Just look below at the pictures of our merle pups this year and you will see. Why not to breed merle to sable or fawn.
First of all they are very hard to spot. Because, only the sabling has been affected by the merling. Leaving small patches of sabling here or there, with other areas having a blue sheen. Many of the pups in my fawn litter only had sabling on their ears or tails (which were NB or Docked). The Docked tails removing all signs of sabling. Loretta's Sable litter were slightly easier to spot. The blue eyes gave them away too. Loretta had one Cryptic with a blue eye. At first we were surprised to find a clear tan in her litter only to discover it was a Cryptic Merle/Phantom Merle.