CNM & PRA (January 5, 2014)|
|Here is where you can read about Hip Dysplasia,CNM & EIC these tests I consider them Very important to have checked & cleared before breeding is considered. Of course there are a lot of other tests that can be done as well.I try and have the hips,eyes ,EIC & CNM tests are done before a litter is considered,but SOMETIMES things don't happen as you want it to be.|
"Many Breeders still do not realize when they have an affected puppy. They assume it is an accidental birth defect. Since Carriers appear normal, it is impossible to identify them without testing. A small portion of breeders do recognize affected puppies and fear that mentioning it will affect the sales of puppies with their kennel name. Additionally, there are breeders who simply are not willing to accept DNA testing as a useful option."
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.
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.
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 ***
We are in the process of testing all our rat terriers. Some have already been tested...Tests are easy to order and administer. Just follow directions carefully and sumit.
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...||690 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.