:
Unfortunately, there is no such thing as a perfect dog of ANY breed. Canine geneticists estimate that the average purebred dog is carrying at least 4-5 defective genes?. even grand champions. Today?s breeders make the best breeding decisions they can based upon testing results, conformation, temperament, working ability, pedigree, etc. A good breeder is open and honest about the health status of all their dogs and is always willing to help and guide the new puppy owner.
Over 350 inherited diseases have been recognized in dogs. The threat of a health problem is not a reason to avoid a breed. All breeds have their genetic traits and these traits should only inspire you to be more careful in selecting the breeder to insure that bloodlines are as defect-free as possible.
Many inherited diseases are restricted to particular breeds but others, such as hip dysphasia, occur in a wide range of breeds. The more common diseases which affect
Dobermans are cervical spondylitis (Wobbler Syndrome), von Willebrand's Disease and thyroid disease. Cancer, hip dysplasia, heart problems, eye defects, skin diseases and chronic active hepatitis (CAH) are also problems which are found in Dobermans. von Willebrand's Disease is one of the least destructive diseases inherited by Dobermans but it should not be ignored. It is a genetically inherited autosomal recessive bleeding disorder much like hemophilia and is the most common bleeding disorder in canines and in humans. It affects some 60 different breeds of dogs including the Doberman Pinscher and, because it is genetic in nature, there is no cure only eradication by deliberate breeding strategies. It is passed on directly from one generation to the next and will affect offspring to varying degrees. The likelihood is that the offspring will be affected more severely than the parents.
Although Dobermans are one of the breeds most commonly affected by von Willebrand's, they usually have only the milder form (Type I). Other breeds suffer from type II (moderate to severe form and extremely rare being found only in German Shorthaired Pointers and
German Wirehaired Pointers) and still others are well known to suffer from type III (severe but rare).
According to information I received from VetGen, since Dobermans inherit the type I form of the disease, homozygous affected puppies (those which inherit a defective gene from both parents) are not likely to die in utero or soon after death as may occur with the more severe type II and type III forms. Both heterozygous Doberman puppies (those inheriting a defective gene from only one parent) and homozygous puppies usually survive quite well.
Further, since von Willebrand?s Disease is recessive, penetrance does not play a role in inheritance.
Under normal circumstances, type I means that bleeding will clot normally. However, in times of stress or with major blood loss during surgery or as a result of trauma, the defect may become ?clinically? apparent with the inability to clot. Bleeding tendencies can be exacerbated by medications or by stress such as illness, particularly viral disease since viral infections can prolong clotting times by impairing platelet cohesiveness and/or endothelial cell production in the blood vessel walls (the endothelial cells produce the protein called von
Willebrand's factor which is necessary for normal clotting). Because Parvovirus attacks the gastrointestinal tract where it causes bleeding, it is especially dangerous to Dobermans.
Live virus vaccines can have the same effect.
There are 3 classifications of type I vWD dogs: Clear, Carrier and Affected. As of January
2004, VetGen states that of the Dobermans it has tested, 25% of Dobermans were classified as clear, 49% were carriers and 26% were classified as affected.
Clears:
A clear Doberman completely lacks the vWD gene and, if bred with another clear Doberman, will produce offspring which will be completely free of the gene. However, since such a small group of Dobermans are designated as clear, exclusive inter-breeding of clears may only rob the Doberman of many of it?s highly desirable characteristics and will probably cause other genetic problems to become more prevalent because other genetic disorders affect this and most other pure bred dogs. Therefore, most breeders recommend that clear to carrier breeding be continued. Affected dogs should be spayed, neutered or bred only to

clears. Breeding a carrier to a clear will result in 100% carriers which are considered by most breeders to be acceptable. Affected dogs should not be ?put down? because many, if not most, will live long, healthy lives with the proper attention to care.
Dobermans which are found to be ?Clear? of von Willebrand?s genes can be quite hard to find. The disease CAN be bred out of a kennel?s bloodline if the breeder is diligent but it is very time consuming and expensive to do so since obtaining a clear female is very expensive and the stud fees for breeding services for a clear male can cost several thousand dollars. Accordingly, such puppies are much more expensive to purchase. The following table illustrates a breeder?s strategy for autosomal recessive diseases such as von
Willebrand's Disease:
Breeding Pair
Combinations
Clear Male Carrier Male Affected Male
Clear Female
Carrier Female
100%
Clear
50/50
Carrier / Clear
50/50
Carrier / Clear
25/50/25
Clear/Carrier/Affected
100%
Carrier
50/50
Carrier / Affected
Affected Female
100%
Carrier
50/50
Carrier / Affected
100%
Affected
Carriers:
Carriers possess only the gene and are unlikely to ever be affected by symptoms. Carriers of the vWD gene are at little or no risk of bleeding from the disease but will transmit the gene to 50% of its offspring. Clear to clear and clear to carrier breeding tends to reduce the appearance of the gene since even carriers will produce 50% clear puppies if bred to a clear or 50% carriers and 25% clears if bred to another carrier. It's simple genetics!
Affecteds:
Affected dogs blood severely or entirely lacks von Willebrand factor (vWF) which is a protein which helps to promote blood clotting by increasing platelet cohesion. von Willebrand's disease doesn?t lower the number of platelets available, it simply makes them less ?sticky? so they are unable to accomplish normal clotting.
An affected pup my bleed from its gums when teething, may have spontaneous nosebleeds, blood in its stool or urine, have excessive bleeding during estrus or after whelping, experience prolonged estrus, have blood in its gastrointestinal tract or it may display prolonged bleeding from small or superficial wounds which can lead to anemia, shock, or, if left untreated, even death. Accordingly, you might request that your vet keep desomepressin, and, at times of scheduled surgery, fresh frozen plasma or cryoprecipitate
(a clotting enhancer) on hand. In an emergency, a transfusion of blood or fresh frozen plasma may stabilize the injured dog. The dog donating the blood may be treated with a drug called DDAVP prior to donation which will raise the amount of von Willebrand's factor in the donor?s blood to make the blood more likely to help the recipient clot more readily.
Affected dogs can have injuries and surgeries without ANY complications and never have a bleeding problem. Why some dogs classified as affected display clinical signs of bleeding while others do not is not yet well understood. Many Doberman owners report that their dog underwent routine spaying, neutering, ear cropping and tail docking as a puppy with an uncomplicated recovery from such procedures but this does not eliminate the possibility that a dog may be affected since some dogs do not become obvious ?bleeders? until later in life. If not tested during puppyhood, genetic affectation usually becomes apparent at about
4 years of age.
Not all dogs will actually bleed, or they may do so only sometimes. von Willebrand's factor status can alter during an animal?s life so that an older dog may show a higher or lower reading than might have been the case earlier in life. A previous non-bleeder can become a bleeder or the percentage of the von Willebrand's factor in the blood can be raised by such events as estrus and pregnancies. Since the disorder often diminishes with age and can therefore result in false-negative results, testing should be done at an early age.
Acquired von Willebrand?s:
In addition to the congenital (inherited) variety of vWD, an acquired (not born with it)

version has also been reported and is associated with hypothyroidism. Auto-immune diseases (in which the body's antibodies attack the body itself) like hypothyroidism inhibit the production and function of von Willebrand's factor in the blood. Some researches claim that both inherited and acquired vWD is a secondary result of auto-imumune thyroid disease and that finding low or low-normal levels of vWD and/or platelet numbers may be an early indication of thyroid disease. If a dog has congenital vWD, their bleeding tendencies can become clinically severe when hypothyroidism is present.
Those dogs with acquired von Willebrand's disease caused by hypothyroidism are best treated with thyroid hormone supplementation (thyroxin) daily for the rest of their lives.
Thyroid supplementation is also frequently prescribed for inherited vWD but such treatment is not always successful. Hyperthyroid dogs can also exhibit low platelet count.
ELISA Testing for von Willebrand's Disease:
In the past, the buccal mucosal bleeding time test and the ELISA (enzyme-linked immunoabsorbent assay) test were about the only diagnostic tools available to differentiate between clear carrier and affected Dobermans. Both measure the levels of von Willebrand's factor in the blood. The mucosal test is not reliable because it is not specific for vWD since bleeding times are also prolonged in dogs with thrombocytopenia (low platelet count) or with platelet functional defects.
ELISA testing can be done as early as 7-8 weeks and runs about $60. Blood levels of vWD vary daily in normal, healthy dogs and is exaggerated in dogs which are in estrus or pregnant and in dogs with a systemic illness (especially liver disease) or in those with inflammatory disorders. The von Willebrand's factor protein is also easily damaged during testing. The more protein which is damaged, the less reliable will be the test.
The ELISA blood test has been reported to have a misclassification rate of less than 5% but breeders know that the results can vary widely from day to day and do not rely heavily upon it. If using the ELISA test breeders know that they must test more than once in a lifetime.
In Dobermans a vWF ELISA test result of 36% or above is usually adequate to prevent excessive bleeding. Levels of 10-20% may adequate to prevent excessive bleeding for mild events such as neutering. Major events such as trauma followed by major surgery may exhaust the vWF in animals which have higher assays including some carriers.
Factors which will help improve the reliability of ELISA testing:
The dog should be healthy, unstressed and should not have been on medication (including steroids or antibiotics) for 60 days. Females should be tested in mid-cycle (90 days after estrus ends) and not while pregnant, lactating or in estrus. Males should not be tested while breeding since hormones and adrenaline can affect the test?s results. Also vaccinations should not be given 2 weeks prior to testing and it is advisable to wait 2 weeks to test after any blood transfusions or surgeries.
Factors which will not affect ELISA test results:
Age (tests results may vary slightly over time but usually not enough to change the status of the dog), gender, worming medications, heartworm medications, flea/tick medications or diet (type of feed being used).
VetGen Testing for von Willebrand?s Disease:
The newer and completely accurate VetGen DNA test can be performed at any age since
DNA is present at birth and does not change throughout the dog?s life. It costs about $150 and is necessary only once.
Medicating an Affected Dog:
Certain medications can precipitate a bleeding crisis in affected dogs and it is critical that they be avoided. The list includes: Nsaids (such as Aspirin, Phenylbutazone, Ibuprofen and
Indomethacin), Estrogen, the cillins (Penicillin, Ampicillin/Amoxicillin), Sulfa-based antibiotics, Phenothiazine tranquilizers, Theophylline, Antihistamines, and Chloramphenical.
Drugs which can induce hemorrhagic disease include at least 10 antibiotics, 8 antimicrobials, 5 anti-convulsants, 7 anti-inflammatory agents, 12 anti-cancer drugs, 7 cardiovascular medications, 1 diuretic, 1 hormone (estrogen), and 12 in the miscellaneous

category. There are undoubtedly more and who knows about drugs used in combination with the seemingly endless array of alternative medical therapies? One combination we do know about and which should ALWAYS be avoided is aspirin-related products (such as
Rimadyl, Ascriptin, etc.) and steroids (such as Prednisone, Dexamethasone, etc.). No over the counter drugs should EVER be used in combination with prescription drugs without the approval of your vet. Low platelet counts can result from diseases of the spleen and liver or from any of several types of cancer as well as occurring secondary to protein-losing processes, inflammation of blood vessels, (allergic and auto-immune, and the frequently fatal disseminated intravascular coagulation (DIC).
Hip Dysplasia:
Hip dysphasia (improper growth of the hip) is both polygenetic (some researchers speculate that there may be as many as 13 genes involved) and multifactorial (influenced by many non-genetic factors) so it is understandably very difficult to reliably breed away from.
Efforts to control this condition date back to the 1960?s.
It is more common in large breeds and results in a hip socket (acetabulum) which is too shallow to properly seat the femoral ball (at the top of the leg where it joins to the hip) or in a femoral ball or femoral neck which is deformed or small causing excessive movement at the hip joint. This condition causes gradual loss of cartilage, bone spurs and the joint to eventually become inflamed and weakened. Dogs with hip dysphasia appear to be born with normal hips and then to develop the disease later. The hip joint is not the only area of the dog which can be affected. Knee, shoulder and spinal joints can also show evidence of changes.
The degree to which the dog exhibits symptoms depends upon many factors such as the strength of the muscle and ligament which help hold the joint in place. It can vary in severity from mild to completely debilitating. Other factors include rapid growth and weight gain which can stress the young joint.
Studies have proven that dysplastic puppies whose diet is controlled in order to slow growth and weight gain may display no outward sign of the condition and may remain functional despite severe dysphasia. This approach allows the muscles and ligaments to develop enough to compensate for bone failure. Some people believe that they can cause dysplasia in their dog by too much exercise however, most vets agree that this is not the case. In other words, how you raise your puppy won't determine whether or not your puppy is dysplastic, but it can affect when and, perhaps whether, he begins to develop symptoms as well as their severity. Some factors which may hasten or worsen symptoms include rough play, jumping, climbing stairs, slick floors, excess weight gain or rapid growth and calcium supplementation which may increase bone remodeling.
If the condition is identified early and is mild, good food and exercise can help the dog remain relatively pain-free. For more moderate cases, surgery can correct the abnormality.
Surgery provides more comfort than medications although it is an expensive option. For very severe cases, in many instances, it may be more humane to have the dog put down.
Several surgical procedures exist to treat hip dysplasia. Each procedure has its pros and cons and different surgeons may have differing levels of experience with each procedure.
Before advanced remodeling of the joint has taken place, the most often recommended surgical treatment for dysplasia is the triple pelvic osteotomy. This procedure must be done before the acetabulum has been worn down and is therefore usually recommended for young dogs under 9 months of age who have clinically diagnosed subluxations. It involves cutting the pelvis in 3 places and then tilting the bone to a more favorable angle to keep the femoral head in place. A somewhat similar option is the inter-trochanteric osteotomy which changes the length and angle of the femoral head. Approximate costs for the procedures are around $800-$1000 per hip.
If there is already extensive damage to the joint, other options include the shelf arthroplasty procedure, femoral head and neck excision or a total hip replacement:
The shelf procedure seeks to extend the rim of the joint thus improving stability. It is somewhat controversial because it does not halt the progress of arthritic changes so the animal may continue to have worsening pain.
The femoral head and neck excision involves removing both the head and neck of the femur. A "sling" of muscles are then used to support and cushion the femoral shaft. This procedure has the best chance of success in dogs weighing less than 50 pounds. Because the bone is shortened, the dog's gait will be affected and so this procedure should be

considered and end-stage salvage procedure. Costs are usually much lower then other types of surgery.
Total hip replacement involves replacing the head and neck of the femur and the acetabulum with prosthetics. This procedure should be reserved for dogs who have reached full adulthood thus negating the possibility of further bone growth which will affect the replacement. It is quite costly (averaging around $1500 per hip) but the prosthesis can be expected to last for life and the dog can bear weight soon after the surgery.
Testing for Hip Dysplasia:
OFA X-ray testing can be done at 2 years of age and the dog's x-rays can be sent to the
Orthopedic Foundation for Animals (OFA) for subjective analysis by three veterinary radiologists and to have their results (excellent, good or fair) registered on that site
(OFFA.org). Recent work has indicated that the standard ?hip extended? view used by OFA may mask hip looseness. It can probably accurately detect dysplasia once secondary changes occur, but is also probably less accurate in detecting only joint laxity which is a reliable predictor of dysplasia. Still, it remains the customary standard by which dogs are graded.
The Penn-Hip method of evaluation requires 3 x-rays with the hip in different positions.
Each hip is then measured mathematically to determine how loose or tight it is using a technique called "compression/distraction". In this procedure, the hips are compressed to determine where the center of the femoral head and the acetabulum coincide. The hips are then distracted using a special device and the distance the head can be moved away from the center is measured. This measurement is called the distraction index (or DI). The DI will range from 0 to 1. Through research, it is postulated that a DI of .03 or lower indicates that the dog is negative for hip dysplasia. Between .03 and .07 is somewhat inconclusive. A DI of
.07 or above is associated with a greater incidence of degenerative hip disease.
While more expensive at approximately $150, its advantages are that it produces objective results (actual measurement) rather than the subjective results (observation and estimation) obtained by OFA certification and its ability to be fairly accurate on puppies as young as young as 16 weeks. OFA is valuable too, but Penn-Hip gives more accurate information and likely will be ?state of the art? until genetic markers are identified and DNA testing becomes available.
No one truly knows how widespread hip dysplasia is in the Doberman population but it seems to be much less prevalent than in many other purebreds. It is rare in the very top quality dobermans but somewhat more common in the rest. Fortunately, hip dysplasia in
Dobermans has been on the decline in recent years thanks to the diligent efforts of reputable breeders to avoid breeding animals with poor OFA ratings.
Testing for other inherited defects:
Cardiomyopathy:
Cardiomyopathy is a general medical term meaning ?disease of the heart muscle? and can have as its cause drugs, toxins, poor blood supply, metabolic disorders (like diabetes), nutrition, infections (viral, bacterial, fungal and protozoan) to name a few. Doberman cardiomyopathy represents a separate and distinct genetic cause added to the list of possible causes.
In the Doberman, it is primarily a genetic trait which results in an inability of the heart to contract normally which leads to abnormal heart function. To compensate for the heart's poor contractile ability, the heart dilates increasing the chamber size which, in the early stages of the disease, will improve output of the heart (stroke volume). At this time the disease is asymptomatic. With further progression of the disease, there will eventually come a time when further dilation of the heart no longer improves stroke volume but, in fact, leads to increasing pressure within the heart. This, in turn, causes a backing up of blood in the blood vessels and lungs which causes fluid to leak out into the lungs leading to difficulty breathing and, eventually, death.
Symptoms and progression vary widely. Some dogs will have no visible symptoms and yet die without warning. We are seeing this more and more in dogs as young as 3 years. Other dogs will display heavy breathing, wheezing, coughing, loss of energy and appetite. The condition is not curable although diuretics and other medications can provide some measure of comfort for the dog. Typical life expectancy for a Dobie diagnosed with this condition is 6 additional months; for other breeds, its somewhat longer. Our advice is to be unselfish and not try to hold on to the dog after it no longer enjoys being a dog.

Another potential cause of death is arrhythmia. With the abnormal stretching of the heart, electrical impulses which govern heartbeat can become abnormal. Some of these abnormalities are benign but others are malignant and result in the death of the dog.
No tests currently exist which can predict Dilated Cardiomyopathy (DCM) or test for it genetically. Unfortunately, the most common sign of DCM is sudden death. An echocardiogram or a heart ultrasound can give you information concerning current heart health but can test results can be normal one year and show signs of cardiomyopathy the next. The best you can probably do it to ask the breeder about ages and causes of death of the ancestors listed in your puppy?s pedigree. Holter monitoring (a 24 hour continuous
ECG) is now available worldwide.
Wobbler?s Syndrome (Cervical Vertebral Instability or CVI):
The term Wobbler's disease has become common usage for CVI because of the distinctive gait displayed by dogs with CVI. This disease causes neck vertebrae (usually at the base of the neck in Dobermans in vertebrae C5, C6, or C7) to become unstable and to move around resulting in pinching of the spinal cord. Although it is most commonly found in the neck, it can affect any part of the body. It's quite common in Dobies.
Perhaps the weakest part of the Doberman is its neck, so easing strain on the neck is beneficial before any damage has even occurred. Putting a pinch collar, Halti, or body harness on a dog that pulls hard on its leash is recommended. The first symptom is often an uneven gait, as if the dog's front end is trying to move faster than the rear. What is occurring is that a disk in the dog's neck is becoming herniated and putting pressure on the spinal cord, causing loss of feeling from the neck back.
The condition is generally not painful, at least not in its early stages. As the dog becomes more paralyzed, foot-dragging, stumbling, difficulty in getting up, and loss of urinary and bowel functions may occur. No one can definitively say what causes CVI however vets usually see more of this disease in certain breeds so this has lead them to believe there must be some type of hereditary basis. Although CVI is thought to be due to genetic inheritance, it cannot be tested for reliably. It rarely strikes until middle age (3+ years) or older and usually causes pain and/or paralysis. Once the dog has lost deep pain reflex, the chances of recovery are basically non-existent.
Diagnosis can be made with a procedure called a myelogram. It is a fairly invasive procedure so an owner should be very cautious and have it administered by a very experienced vet. Adverse effects of poorly performed myelograms can be devastating and, in some cases, worse than the original disease. A less invasive alternative diagnostic tool,
Magnetic Resonance Imaging (MRI), is now available through most specialty vet practices.
While there is no cure for CVI, surgical intervention can stabilize the affected area but it must be done at the first onset of the disease. We do NOT, in general, recommend surgery for this condition. It is expensive, has a 3 to 10 months long recuperation period, and is not believed to reverse any damage that has already occurred which means the dog probably will not get BETTER. Short-term relief may be provided by corticosteroid medications, which help to relieve the pressure.
Hypothyroidism:
Antibodies are proteins designed to defend the body from foreign organisms such as bacteria and viruses. In autoimmune hypothyroidism, antibodies attack and destroy thyroid gland cells preventing the gland from being able to release normal amounts of thyroid hormone.
In Dobermans, hypothyroidism is usually always an autoimmune disorder of the thyroid gland, but the mode of transmission and inheritability is unknown. A female with antithyroid antibodies in her blood may pass these along to her puppies in her colostral milk and any dog having circulating anti-thyroid antibodies can eventually develop clinical symptoms of hypothyroidism or other autoimmune diseases.
The term hypothyroidism has been loosely applied to describe all stages of this disease process whereas, strictly speaking, it should be reserved for the end-stages when the animal?s thyroid gland is no longer capable of producing sufficient hormones to sustain clinical health. At this point, the dog can express any number of the non-specific, multisystem signs of thyroid dysfunction. Autoimmune thyroiditis accounts for an estimated 90% of thyroid cases.
Symptoms of hypothyroidism may include, droopy eyes, a "tragic" facial expression, muscle wasting of head and/or body, lethargy, fatigue, weight gain, thinning of hair along the back

("razor back"), disruption of reproductive seasons, females failing to impregnate and/or carry to term and temperament changes. It is also frequently linked to adrenal insufficiency, allergies, hives, dry skin, vomiting and intolerance to cold or heat. Hyperactivity (overactive thyroid), weight loss and aggression can occur with hyperthyroidism.
Hypothyroidism develops in genetically susceptible animals and is characterized by the presence of anti-thyroid antibodies in the blood or tissues. In most cases, it starts around puberty and gradually progress through mid-life and old age to become clinically expressed hypothyroidism once the thyroid glandular reserves have been depleted. During the progression of the disease, the animal becomes more susceptible to other diseases (like von
Willebrand?s).
Thyroid screening is less likely to be meaningful before puberty. Therefore, testing should commence once healthy dogs have reached sexual maturity (usually between 9 and 14 months in males and following the first estrus cycles in females).
Thyroid titers should be done every 18 to 24 months throughout a dog?s life. Fortunately, this disease is easy and inexpensive to treat. Thyroid disease (more prevalent in older dogs) will affect ELISA testing so it?s best to have the dog tested for thyroid dysfunction prior to
ELISA testing for vWD.
Inherited Eye defects:
Dogs can inherit a variety of eye disorders and can be examined by CERF (Canine Eye
Registration Foundation) certified canine opthalmologists for inherited eye defects.
Fortunately, dobermans are fairly free of inherited eye disease with the most common being cataracts (which occur prior to 2 years of age and have not been conclusively shown to be an inherited trait) as well as microopthalmia (very small eyes) and persistent pupillary membrane.... all of which are rare. CERF certification is only good for one year so must be done annually to be kept current.
White (Albino) Dobermans:
In the United States, there are four accepted colors in the Doberman breed. These are black, red (also referred to as brown), blue, and fawn (also referred to as Isabella). In the
Doberman breed there are only two sets of genes which interact to produce these colors -- the "B" series, and the "D" series. Each of these gene "series" contains two alleles (variants) in the Doberman breed; the "dominant" allele is referred to with a capital letter, while the
"recessive" allele is referred to with a lower-case letter. Dominant alleles always
"dominate", or hide, the effects of recessive alleles in the same gene series. So we have B, b, D, and d. B produces black, b produces red (brown), D produces full pigment (nondilute), and d produces dilute pigment.
Each dog carries two copies of the B series of genes and two copies of the D series of genes, and the dominant allele will always cover the effect of the recessive allele. So a black dog can be either BB or Bb, but a red dog must be bb. Similarly, a dog with non-dilute pigment can be either DD or Dd, but a dog with dilute pigment must be dd. Blue dogs are the dilute form of black, and fawn dogs are the dilute form of red.
So here's what we're left with --
Black dogs can be BBDD BbDD BBDd BbDd
Red dogs can be
Blue dogs can be bbDD
BBdd bbDd
Bbdd
Fawn dogs can ONLY be bbdd
Therefore, the albino trait is not dominant to either the black or dilution traits. This means that a dog must carry two copies of the albino gene in order to hide the other color traits.
Breedings prove that the albino trait is not in the same gene series as either the black trait or the dilution trait. The albino trait must therefore be inherited at a separate site. Further, albino/fawn breeding also proves that the albino trait in Dobermans is "epistatic" -- which means that it covers or "masks" the effect of both the black and dilution traits when the dog has two copies of the albino gene. Further, breedings have proven that the albino variant in dobermans is inherited as a simple recessive trait. If an albino involved in an albino/fawn breeding had both the dominant black and the dominant non-dilution trait, it would produce a black dog if there were no albino genes present. If it had two copies of the albino gene, both the black and non-dilution genes would be "masked" or "hidden". That's why the albino gene is often referred to as a "masking gene".

We now know that defects in several different genes can produce albinism. The albino series of genes is classically referred to as "C". Therefore, all albino dogs must carry two copies of the recessive gene, cc in order to appear albinistic. Normally colored dogs can be either CC or Cc. Dogs who are Cc can be any of the accepted colors, and there is currently no test
(except for test breeding) which will detect the albino gene being carried by these dogs.
The results after a five-year study conducted by the DPCA and its consultants, concluded these mutants were correctly termed, "albino? (tyrosine positive) or ?partial albino?
(tyrosine negative). It is important to note here that partial albinos are still albinos.
Although albino Dobermans are not permitted in the show ring, their normally-colored siblings ARE.
While we definitely do not agree with those who intentionally breed for white Dobermans, neither do we agree with those who believe that all dogs carrying the recessive gene for albinism should be spayed or neutered. There are several sound reasons behind our opinion.
In Summary:
Since, like every dog, whether purebred or mixed breed, Dobermans can have health issues, the knowledgeable breeder will strive to minimize those over which they can exert some control. They will be open to prospective buyers about their dogs health histories and test results and will always be willing to help the new owner to learn everything they can about their dog.
Because there are no reliable tests for some disorders like CVI and cardiomyopathy and tests for others are not always reliable while still others can be normal at one test and abnormal at the next (like eye disorders and thyroid disease), a breeder has limited control over freeing his kennel from them. For those, he relies upon feedback from the dogs owners over the lifespan of the dogs he provides from his kennel as much as he does testing.
Over the last decade, scientists have begun to identify individual genes and DNA-based technology has been developed to test animals for the presence of disease-causing genes.
Some disorders, such as vWD and hip displasia, are genetic and can be reliably tested and accounted for in the breeding practices of the kennel over time. For the others which can't, progress is still being made.