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von
Willebrand's Disease
(vWD)
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von Willebrand's Disease (vWD) is an inherited condition that may result in an animal to bleed. This bleeding may be of a varying tendency and severity between affected individuals. In dogs it may be an acquired condition associated with an underlying disease, but is most commonly seen as an inherited condition. Acquired forms of the disease are often susceptible to treatment of the underlying disease, the concentration of von Willebrand Factor (vWF) returning to normal in many cases.
For those animals with the inherited condition there is no possibility of a cure. When aware of a decrease in vWF concentration, informed breeders, owners and their veterinarians can be aware of the possibility of complications due to accident, injury and/or surgery and propagation of this trait can be reduced or eliminated by informed breeding decisions.
von
Willebrand's
Disease results in a reduced quantity and/or function of von
Willebrand's
factor (vWF), a glycoprotein necessary for normal platelet function in
the
initial phase of haemostasis (blood clotting). It is caused by the
inheritance
of mutated genes that code for the production of von Willebrand Factor,
these
mutated genes are also referred to as the von Willebrand's Disease
genes.
von Willebrand's Disease is inherited as an autosomal recessive trait.
This
means an animal (male or female) with two mutated vWF genes will be
affected
with the disease. An animal who has inherited 1 mutated gene will be a
carrier
of von Willebrand's Disease. If 2 carrier animals are mated, there is a
probability
that half of the resulting offspring will be carriers, 25% will be
affected
with the disease, and 25% will be normal. There is variable expression
of
the vWF trait, so some affected animals may bleed severely while other
affected
animals may hardly show any bleeding at all. Therefore, we can not
reliably
predict which dogs with low plasma vWF concentrations will show
impairment
of haemostasis.
Breeds of
dogs
with a high prevalence of the vWD gene (15-80%) include the Basset
Hound;
standard and miniature Dachshund; Doberman Pinscher; German Shepherd;
Golden
Retriever; Keeshond; standard and toy Manchester Terrier; miniature
Schnauzer;
Pembroke Welsh Corgi; miniature and standard Poodle; Rottweiler;
Scottish
Terrier and Shetland Sheepdog. Von Willebrand’s Disease has been
documented
in other breeds and/or cross bred dogs, but the prevalence of the vWD
gene
is lower than 15% or insufficient data has been accumulated in order to
determine
prevalence.
Clinical
signs
of bleeding that are typical of the decrease in platelet function seen
with
vWD include bleeding from the gums, urinary system, epistaxis (nose
bleed)
and/or gastrointestinal bleeding, with or without diarrhoea.
Petechiae
(small haemorrhages) on the gums or any mucosal surfaces may be
apparent.
Animals with vWD may be prone to prolonged bleeding at any site of
injury,
trauma or surgery. Haemorrhage into body cavities, joints or
large
extravasations are more suggestive of other coagulation factor
deficiencies, but do not rule out the presence of vWD.
Not all
animals
with decreased levels of vWF exhibit increased tendency to bleed.
Obtaining
a buccal mucosal bleeding time may be of benefit in determining if an
individual
with decreased vWF concentration is likely to exhibit clinical signs of
bleeding,
with or without trauma. Buccal mucosal bleeding time may be used
to
help formulate classification and recommendations for breeding (See
Interpretation
section). Surgicutt buccal mucosal bleeding time devices
are
available from Diagnostic Laboratory Services at the cost of
£10.00.
Instructions and expected bleeding times are supplied with the device.
Method
of
Testing
Animal
Health
Trust refers samples to Cornell University, New York for testing by the
Enzyme-Linked
Immunosorbent Assay (ELISA) method for vWF determination in blood
plasma.
It compares patient vWF antigen concentration to that of a known canine
standard.
Animal
Health
Trust offers a genetic test for von Willebrand’s disease, which carried
out
at our Newmarket site. This test is only available for Irish Red
&
White Setters. For more information contact our Canine Genetics
Group
on 08700 509144, or visit the AHT website: www.aht.org.uk.
In healthy
animals
the vWF concentration may be used to predict genetic status with regard
to
vWD. Heterozygous carriers of vWD usually are identified as
having
less than half the normal concentration of plasma vWF. The
homozygous
condition results in production of little or no vWF protein.
There is a
borderline
level of vWF concentration (50-69%) at which accurate prediction of vWD
status
is not possible. It may be the result of normal genotype or
heterozygous
carrier of the vWD gene. Retesting and/or breeding only to higher
testing
mates is recommended and puppies should be checked.
The rate
of
misclassification of genetic status by the ELISA test has been reported
to
be less than 5%. However, misclassification of genotype by false
positive
or false negative result is always possible. Retesting of an
additional,
freshly drawn sample is recommended in any animal with a result
suspected
of being falsely positive or negative. In addition, analysis of
samples
from the parents of progeny affected with vWD is recommended,
regardless
of their previous status - they may have been misclassified as free
from
vWD. Review of sample collection, handling and testing
conditions, as
well as animal condition, possible health problems and recent
medications also should be considered.
Ageing
of
Samples
Studies of sample stability while frozen at -20oC for 1 week indicate no significant decrease in vWF concentration during this time.This is important since thawing of plasma samples during prolonged transport may cause decreases that would change the interpretation of the test results.
Ageing of the
sample may affect vWF levels, as may repeat freezing and thawing.Our
studies
of sample ageing at room temperature over
1 - 12 days indicate a
decline
in vWF concentration of up to 37%. Decreases of up to 18% may
occur
with only 2 days at room temperature with progressive, but smaller
decreases
occurring up to 7 days. After 7 days there appears to be more
variation
in levels with possible plateau effect.Studies of sample stability while frozen at -20oC for 1 week indicate no significant decrease in vWF concentration during this time.This is important since thawing of plasma samples during prolonged transport may cause decreases that would change the interpretation of the test results.
Indications
for Testing
The vWF
test
is indicated in dogs in the following circumstances:
Prior
to
breeding.
Animals
known
to be at risk for vWD based on breed, clinical signs and/or history
should
be tested. In a healthy animal, vWF concentration may be used to
predict
genetic status.
In
conjunction
with other tests in animals with clinical signs of bleeding, conditions
that
may predispose to acquired vWD or other causes of bleeding.
Conditions
Contraindicating Submission of Samples for vWF Screening
The
concentration
von Willebrand Factor may be influenced by a variety of hormones,
medications
and inflammatory conditions. This may result in unpredictable
fluctuations
of vWF concentrations. Samples for vWF testing should not be
collected
if the following apply.
Vaccination,
medication (including steroids) or resolution of systemic illness
within
the last 2 weeks.
Recent
blood
transfusion, within the last week.
Recent
surgery,
as vWF may participate as an acute-phase reactant protein and increase
with
inflammation or stress. This test should be scheduled prior to surgery
if
there is concern about increased risk associated with breed, clinical
signs
or history.
Pregnancy,
oestrus
(heat) or lactation. An anoestrus sample is recommended for
female
dogs.
Suspected
endocrine
disease that has not been evaluated.
Hypothyroidism
may aggravate decreases in vWF. Other endocrine conditions may
influence vWF concentrations. Concurrent evaluations of endocrine and
vWF status may be of benefit in some individuals, based on clinical
signs, presentation and
history.
We also
recommend
that puppies are tested at least 2 weeks after their ‘last’
vaccination.
Sample
Collection
& Handling
Careful
collection
and handling are critical in obtaining an accurate result. With
improper
sample collection there may be early activation of haemostasis prior to
the
visual detection of a clot, which tends to produce falsely low vWF
concentration
results.
Sodium
citrate
is the only suitable anti-coagulant for von Willebrand Factor testing.
Use only
plastic
syringes and tubes, as glass tends to cause activation of haemostasis
resulting
in the formation of a clot.The correct ratio of citrate anticoagulant
(3.8%
Tri-sodium citrate) to blood is important, so the tube(s) should not be
under
or over-filled.
Usually
collection
of a minimum volume of 2.0 ml of blood is requested to ensure that an
adequate
volume of plasma is obtained.
Remove the
needle
from the syringe and gently expel blood down the side of a plastic
sodium
citrate tube. Do not squirt blood through the needle as this may result
in
the destruction of red blood cells.
The sample
must
be mixed gently but thoroughly immediately after collection, to prevent
activation
of haemostasis, that may cause a falsely low of von Willebrand Factor
result.
If a clot
is
present, the sample is not suitable for submission and should be
recollected.
Prompt
centrifugation
and separation of plasma from the blood cells is requested if possible.
Since
prolonged contact of cells and plasma may result in haemolysis, or
transcellular
shifts of constituents that may interfere with the testing or reduce
the
volume of plasma available for harvesting.
If your
sodium
citrate sample tube will not fit into your centrifuge, transfer the
blood
to an appropriately sized, clean, plain plastic tube (no
anti-coagulant) for
centrifugation. The sample should be centrifuged at 2000-3000 rpm for
10
minutes or using the settings that you usually use to separate blood in
your
centrifuge.
If
excessive
haemolysis is present, in the plasma after centrifugation the sample
may
not be suitable for testing and recollection is advised.
Carefully
pipette
plasma, taking care that erythrocytes are not aspirated. Use a plastic
pipette
and transfer plasma to a clean, plain, plastic tube that does not
contain
anticoagulant.
Please
label
the tube with the animal and owner name, date and contents (citrated
plasma).
For the
von
Willebrand Factor Antigen test we recommend that the plasma be frozen.
Samples
kept at room temperature have been shown to give lower results compared
to
samples that have been stored refrigerated or frozen.
We
recommend
that the sample is sent to the laboratory by as soon as possible, i.e.
overnight
delivery (by special delivery post or courier). Ice packs should be
included
with the sample packaging for vWF testing to ensure that the sample
remains
cold.
Please do
not
send samples on Friday since the weekend may delay delivery. In this
case
keep the sample frozen and post on Monday.
When
samples
are received for von Willebrand Factor testing, they are stored frozen
until
the next test. Samples are sent to Cornell University, USA
by
courier every other Wednesday with results available by Monday morning.
References
Avgeris, S., Lothrop, CD JR.,
McDonald, TP. Plasma von Willebrand Factor Concentration and Thyroid
Function in Dogs. J. Am. Vet. Med. Assoc. 196: 921-924,
1990.
Benson, RE, Catalfamo, JL, Dodds, WJ. A Multispecies Enzyme-linked Immunosorbent Assay for von Willebrand Factor. J. Lab. Clin. Med. 1119: 420-427, 1992.
Brooks, M., Dodds, WJ, Raymond, SL. Epidemiologic Features of von Willebrand’sDisease in Doberman Pinschers, Scottish Terriers and Shetland Sheepdogs, 260 cases(1984-1988). J. Am. Vet. Med. Assoc. 200: 1123-1127, 1992.
Dodds, J.W. Bleeding Disorders. In: Handbook of Small Animal Practice. 2nd ed. Morgan,R.V. (ed.), Churchill Livingstone Inc., New York, N.Y., 1988, pp. 773 -786, 1992, pp. 765-777.
Dodds, W.J. Contributions and Future Directions of Hemostasis Research. J. Am. Vet. Med. Assoc. 193: 1157-1160, 1988.
Dodds, W.J. Bleeding and Immune Diseases, Parts I and II, and Acquired von Willebrand’s Disease. Proc. 56th Meeting, American Animal Hospital Association, St. Louis, MO, 1989, pp. 606-619.
Dodds, WJ. Hemostasis. In: Clinical Biochemistry of Domestic Animals, 5th ed. Kaneko, JJ, Harvey, JW and Bruss, ML (eds). Academic Press, London, 1997, pp. 241-283.
Johnson, GS, Turrentine, MA, Draus, KH. Canine von Willebrand’s Disease: a Heterogenous Group of Bleeding Disorders. Vet. Clin. North Am. 18: 195-229, 1988.
Green, RA and Thomas, JS. Hemostatic Disorders: Coagulopathies and Thrombosis. In: Textbook of Veterinary Internal Medicine, Ettinger, SJ and Feldman, EC (eds). W.B. Saunders Company, London, 1995, pp. 1952.
Reagan, WJ and Rebar, AH. Platelet Disorders. In: Textbook of Veterinary Internal Medicine, Ettinger, SJ and Feldman, EC (eds). W.B. Saunders Company, London, 1995, pp. 1973-1974.
Benson, RE, Catalfamo, JL, Dodds, WJ. A Multispecies Enzyme-linked Immunosorbent Assay for von Willebrand Factor. J. Lab. Clin. Med. 1119: 420-427, 1992.
Brooks, M., Dodds, WJ, Raymond, SL. Epidemiologic Features of von Willebrand’sDisease in Doberman Pinschers, Scottish Terriers and Shetland Sheepdogs, 260 cases(1984-1988). J. Am. Vet. Med. Assoc. 200: 1123-1127, 1992.
Dodds, J.W. Bleeding Disorders. In: Handbook of Small Animal Practice. 2nd ed. Morgan,R.V. (ed.), Churchill Livingstone Inc., New York, N.Y., 1988, pp. 773 -786, 1992, pp. 765-777.
Dodds, W.J. Contributions and Future Directions of Hemostasis Research. J. Am. Vet. Med. Assoc. 193: 1157-1160, 1988.
Dodds, W.J. Bleeding and Immune Diseases, Parts I and II, and Acquired von Willebrand’s Disease. Proc. 56th Meeting, American Animal Hospital Association, St. Louis, MO, 1989, pp. 606-619.
Dodds, WJ. Hemostasis. In: Clinical Biochemistry of Domestic Animals, 5th ed. Kaneko, JJ, Harvey, JW and Bruss, ML (eds). Academic Press, London, 1997, pp. 241-283.
Johnson, GS, Turrentine, MA, Draus, KH. Canine von Willebrand’s Disease: a Heterogenous Group of Bleeding Disorders. Vet. Clin. North Am. 18: 195-229, 1988.
Green, RA and Thomas, JS. Hemostatic Disorders: Coagulopathies and Thrombosis. In: Textbook of Veterinary Internal Medicine, Ettinger, SJ and Feldman, EC (eds). W.B. Saunders Company, London, 1995, pp. 1952.
Reagan, WJ and Rebar, AH. Platelet Disorders. In: Textbook of Veterinary Internal Medicine, Ettinger, SJ and Feldman, EC (eds). W.B. Saunders Company, London, 1995, pp. 1973-1974.
VON WILLEBRAND'S FACTOR TESTING BY ELISA
Interpretation
of Results
This test is used to screen
animals
for the presence of von Willebrand’s disease (vWD) and can be used as a
tool
for prediction of genetic status in healthy animals used for breeding.
The
Reference Interval for dogs is 70-180%. This means that
individuals
without vWD are expected to exhibit von Willebrand’s Factor (vWF)
concentrations
that vary from 70-180% of that of a standard control.| Patient Result for vWF | |
| > 180% | Interpretation with regard to vWD genetic status not possible. May reflect stress, improper sample collection or handling or activation from concurrent disease. Retesting recommended |
| 80-180% | Within normal limits. Does not support the presence of vWD gene. |
| 70-79% | At the lower end of normal range. Does not support the presence of vWD, but caution advised for breeding. Mating to individuals with higher levels is recommended and puppies should be checked. |
| 50-69% | Borderline result. May be the result of normal status or heterozygous carrier of vWD gene. Recommend retesting and/or breeding only to higher testing mates and checking puppies. |
| 1-50% |
Consistent with heterozygous carrier of vWD gene. If no evidence of bleeding clinically and buccal mucosal bleeding time results are within normal limits, breeding only to higher testing mates is recommended and puppies should be checked. If clinically signs are present and/or buccal mucosal bleeding time is abnormal, animal should not be used for breeding. |
| < 1% | Consistent with homozygous status for vWD gene. This animal is the likely the progeny of 2 asymptomatic, heterozygous carrier parents and should not be used for breeding. |
DNA Studies in Doberman von Willebrand's Disease.
The Mutation Discovered and a DNA Test Developed
by George J. Brewer, Professor,Department of Human Genetics and Internal Medicine,
University of Michigan Medical School, Co-Founder of VetGen LLC
Our
research
team is very excited about our discovery of the mutation that causes
von
Willebrand's disease (vWD) in the Doberman Pinscher. Credit for the
discovery
must include my colleagues, Dr.'s Patrick Venta, Vilma
Yuzbasiyan-Gurkan,
and William Schall, of the College of Veterinary Medicine at Michigan
State
University, and to Dr. Jianping Li, who works in my laboratory at the
University
of Michigan as well as at VetGen LLC, and who did all the DNA
sequencing.
This discovery is a nice example of the productive co-operation between
the
two universities and the company mentioned, as well as four funding
organizations
that provided support, The Doberman Pinscher Foundation of America,
Inc.,
The Orthopaedic Foundation for Animals, the Morris Animal Foundation,
and
the American Kennel Club.
The
mutation
itself has some interesting aspects. For one thing, precisely the same
mutation
has occurred in some human patients with vWD. It is a little unusual to
see
mutations be identical across species. This shows how closely we are
related
to our canine brethren! Second, the mutation is of a type such that
completely
normal von Willebrand's factor (vWF) is made about 5-10% of the time.
Technically,
the mutation is called a splice site mutation, with alternative
splicing
occurring about 90-95% of the time. That jargon won't mean much to the
average
Doberman breeder or owner, but let me explain what is happening in lay
person
language. It may be useful for the Doberman fancy to understand the
mutation
to a certain extent, because its nature explains why it was so
confusing
to understand for a long time, and it also explains why affected
Dobermans
have a milder disease than, say, affected Scotties.
To try to
understand
the effects of this mutation, let's use an analogy common to general
experience.
Imagine that a freight train is supposed to go from point A to point B
following
a railroad track. There is a point where a side track goes to point C.
However,
normally the train never goes to point C, because the switch to point
C,
connecting the track up to the main track, is never thrown. Then the
switch
breaks (this is the mutation) such that the lock holding the switch
from
connecting the track to point C is no longer effective. The switch can
now
jiggle back and forth, sending some trains to point B, and others to
point
C. As freight trains rumble towards the switch, 95% of the time it
jiggles
over and causes the train to end up at point C. This is useless because
point
C ends at a cliff. The trains rumble over the cliff and are never heard
from
again. A minority of the time, maybe about 5%, the switch jiggles the
other
way and the trains end up at their normal destination. So, only 5% of
the
freight is delivered.
This is
exactly
what happens in the Doberman affected animal. These animals have two
doses
(two trains in the above example) of the mutated gene. Each gene is
capable
of making 5-10% of normal vWF (that is, going down the main track to
point
B), because the normal splice site is used a little. The 90-95% of the
time
the mutated splice site is used (going down the side track to point C),
no
useful vWF is produced. Since each of the two mutated genes is
producing
5-10% of normal vWF the affected Doberman ends up with twice that, or
10-20%
of normal vWF in their blood.
So, one of
the
mysteries of Doberman vWD that has puzzled scientists for years, how
affected
dogs can end up with a small amount of completely normal vWF, is
cleared
up by understanding this type of mutation. A second mystery is also
cleared
up. Doberman owners and breeders have had their dogs tested for vWF for
years
using the protein assay of vWF, and have often discovered low values in
dogs
without a bleeding history, even at surgery. The reason is, such dogs
have
10-20% of normal vWF. If the bleeding stress isn't too great, the
10-20%
of normal vWF that is present can prevent undue bleeding. Part of the
time
uneventful surgery fits that criterion, and unusual bleeding does not
occur.
I hasten
to
add that this should not be taken to mean that vWD in the Doberman is
clinically
harmless. The literature is full of reports of Doberman's bleeding and
dying
from vWD. There are a number of factors, known and unknown, which will
affect
the clinical outcome in a given case. First coagulation factors, such
as
vWF, are consumed during blood clotting. The more the bleeding, from
injury
or surgery, the more the consumption, and the more likely the limited
supply
of vWF in an affected Doberman will be used up, leading to renewed
bleeding,
now from vWF deficiency. Second there is also variation in the amount
of
vWF in affected Dobermans. A dog with a 5% value is at greater risk
than
one with 15%. Of course, other factors, such as other coagulation and
tissue
factors that we aren't measuring, will certainly vary from one affected
dog
to another, and change the risk of bleeding up or down in a given
situation.
The Doberman breeder and owner should view vWD as a significant health risk, and a fault, and strive to get rid of the mutated gene. The discovery of the mutation, and the recent development of a DNA test, now provides just that opportunity.
The Doberman breeder and owner should view vWD as a significant health risk, and a fault, and strive to get rid of the mutated gene. The discovery of the mutation, and the recent development of a DNA test, now provides just that opportunity.
Another
mystery
about Doberman vWD that we now understand better is the actual
frequency
of vWD in Dobermans. Dobermans have been said to have a 70% plus
frequency
of this disease, but that is not correct. It's more on the order of 35%
affected,
with an additional large group being carriers, but free of any bleeding
risk.
The disease is an "autosomal recessive", which means that affected
animals
have two doses of the mutated gene, and a mild to moderate risk of
bleeding,
for reasons explained earlier. Based on very preliminary data, we
believe
the mutant gene has a frequency of about 0.6 (60% of the genes are
mutant)
which translates into about 36% of all Dobermans being homozygous
affected
(two doses of the abnormal gene and at risk for bleeding), 48% being
carriers
(one abnormal and one normal gene, no risk of bleeding), and 16% being
homozygous
clear (two doses of the normal gene). If the gene frequency turns out
to
be closer to 0.5, the frequencies for affected will be 25%, carriers
50%,
and clear 25%. Of course, our small sample comes from a limited region
of
the country. The gene frequencies may vary some in different parts of
the
country, but the bottom line will remain the same. This is a very
common
disease and a very common mutant gene.
Carriers of the mutant vWD gene are at no risk of bleeding from vWD, but of course, will transmit the mutant gene to their offspring 50% of the time. Roughly, the ranges of vWF factor levels are 5 to 20% for affected, 30-100% for carriers, and 50-130% for homozygous normal. Note the major overlap between carriers and normals for vWF levels. This overlap accounts for the extreme unreliability of the vWF assay in trying to identify Doberman carriers of vWD.
Carriers of the mutant vWD gene are at no risk of bleeding from vWD, but of course, will transmit the mutant gene to their offspring 50% of the time. Roughly, the ranges of vWF factor levels are 5 to 20% for affected, 30-100% for carriers, and 50-130% for homozygous normal. Note the major overlap between carriers and normals for vWF levels. This overlap accounts for the extreme unreliability of the vWF assay in trying to identify Doberman carriers of vWD.
The new
DNA
test for Doberman vWD is offered by VetGen LLC (3728 Plaza Drive, Suite
1,
Ann Arbor, Michigan 48108; (734) 669-8440, (800) 4-VETGEN; Fax (734)
669-8441).
It is very easy to do the test. You can order the test kit from VetGen
by
phone or letter. Each test kit costs $5 and contains three soft brushes
and
instructions. Following the instructions, the dog owner brushes the
inside
of the dog's mouth. Some of the cells lining the inside of the mouth
stick
to the brush, and provide the DNA for the test. No blood is required.
The
brushes are replaced in their envelope and mailed back to VetGen. Each
vWD
DNA test costs $135. VetGen will supply test results within two weeks
of
receiving the DNA.
Test
results
will come back as "clear," "carrier," or "affected." As stated earlier,
clear
means both vWF genes are normal, carrier means one is normal and one is
defective,
and affected means both genes are defective. It is important to realize
that
this DNA test is very different from the old protein based factor
assay.
The DNA test is definitive and final, a lifelong, permanent
determination
of the vWD status of each dog tested as contrasted to the factor assay,
in
which the levels could change drastically over time. We can now say in
hindsight
that the old test probably correctly identified some affected Dobermans
(values
under 20), but it is completely unreliable for carrier detection.
What
should
a breeder do with the test results, once they are obtained, in terms of
breeding
decisions? The problem facing the Doberman breeder is that it appears
that
only 15 to 20% of Dobermans are clear of the vWD gene. If one breeds
mostly
clear to clear, it narrows the breeding pool so much that there is risk
of
losing some of the Doberman's genetic heritage, i.e., some of the genes
determining
valuable positive characteristics of the Doberman might be lost, or
highly
diluted. Therefore, as a first priority, we advise breeding clear to
clear
and clear to carrier, at least for the next two or three generations.
Over
time, as the frequency of clear dog’s increases, it should be possible
to
breed mostly clear to clear, and to eventually eliminate the mutant vWD
gene.
As a
second
priority, we suggest that it is reasonable to breed carrier to carrier,
if
an acceptable clear dog is not available for breeding. This type of
mating
will produce 25% clear, 50% carrier, and 25% affected, on average. The
puppies
should be tested and the affected puppies not used for breeding.
Breeding carrier to affected and affected to affected should be avoided if at all possible. The first breeding produces 50% affected on average, and the second produces 100% affected animals. In my opinion, there should be two initial objectives of the Doberman vWD breeding program. One objective should be to produce as few affected animals as possible, because each is a health risk. That doesn't mean we believe affected Doberman puppies should be put down. Most of them can live normal lives. If possible, we believe it would be a good idea to neuter affected animals. The second objective of the breeding program should be to gradually reduce the gene and disease frequency. The kinds of breedings involving the mating of an affected, as listed at the first of this paragraph, tend to increase the disease gene frequency, whereas clear to clear and clear to carrier breedings tend to decrease frequency. Click here for further information on Breeding Strategies.
To further raise the awareness and standards of Doberman breeders, VetGen is helping the Orthopaedic Foundation for Animals (OFA) establish a vWD registry for Dobermans. By registering the results of the vWD DNA test on their dogs, breeders stand to benefit at the point of sale when selling either carrier or clear puppies as established by the vWD DNA test.
In summary, Doberman pinscher breeders are now in the advantageous position of being able to begin eliminating one of the significant diseases in their breed, because of the discovery of the mutation producing vWD in this breed, and the development of a vWD DNA test by VetGen. The test is remarkably easy to get done, and is reasonably priced, considering that it is a definitive lifetime determiner of the vWD genetic type of the dog tested. We urge Doberman breeders to get their breeding stock tested, so that we can get on with eliminating this disease.
For further information, or to order test kits, contact VetGen at:
3728 Plaza Drive, Suite 1, Ann Arbor, Michigan 48108
800-4-VETGEN (800-483-8436) / fax 734-669-8441
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Breeding carrier to affected and affected to affected should be avoided if at all possible. The first breeding produces 50% affected on average, and the second produces 100% affected animals. In my opinion, there should be two initial objectives of the Doberman vWD breeding program. One objective should be to produce as few affected animals as possible, because each is a health risk. That doesn't mean we believe affected Doberman puppies should be put down. Most of them can live normal lives. If possible, we believe it would be a good idea to neuter affected animals. The second objective of the breeding program should be to gradually reduce the gene and disease frequency. The kinds of breedings involving the mating of an affected, as listed at the first of this paragraph, tend to increase the disease gene frequency, whereas clear to clear and clear to carrier breedings tend to decrease frequency. Click here for further information on Breeding Strategies.
To further raise the awareness and standards of Doberman breeders, VetGen is helping the Orthopaedic Foundation for Animals (OFA) establish a vWD registry for Dobermans. By registering the results of the vWD DNA test on their dogs, breeders stand to benefit at the point of sale when selling either carrier or clear puppies as established by the vWD DNA test.
In summary, Doberman pinscher breeders are now in the advantageous position of being able to begin eliminating one of the significant diseases in their breed, because of the discovery of the mutation producing vWD in this breed, and the development of a vWD DNA test by VetGen. The test is remarkably easy to get done, and is reasonably priced, considering that it is a definitive lifetime determiner of the vWD genetic type of the dog tested. We urge Doberman breeders to get their breeding stock tested, so that we can get on with eliminating this disease.
For further information, or to order test kits, contact VetGen at:
3728 Plaza Drive, Suite 1, Ann Arbor, Michigan 48108
800-4-VETGEN (800-483-8436) / fax 734-669-8441
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