HYPERTROPHIC OSTEODYSTROPHY - Konrads Story
disease is something that i feel should be
brought to the attention of all breeders who
are unaware of it, in almost 20 years of
breeding i have never come across anything
like it, i hope by reading this information
if you come across HOD you can effectively
treat it without having to go through months
of sleepless nights & trips to the vet while
they kept guessing what the problem with
Konrad could be, everything from upset
stomach, septicaemia, broken pelvis, broken
legs, the list goes on & on from the age of
6 weeks to almost 18 weeks with numerous
x-rays & operations.
ABOUT THE DISEASE
Hypertrophic osteodystrophy causes lameness
& extreme pain in young growing dogs,
usually of a large breed. Great Danes,
G.S.D.s, Dobermanns, Retrievers &
Weimaraners are examples of breeds that may
be affected by this condition. It appears to
occur in Weimaraners as a vaccine reaction &
this may also affect Mastiffs & Great Danes.
this case it usually occurs a few days after
Vaccination and may appear to be worse than
the "average" case on radiograph. ( In
Konrads case he had a high fever & would not
eat, we thought he had got some kind of
virus, he was walking very stiff on both
back legs, he was given painkillers &
antibiotics over 2 weeks & he seemed to
recover, so at 8 weeks he was vaccinated
along with the other pups, after this things
became progressively worse) .
HOD usually shows up as an acute lameness,
often seeming to affect all four legs
simultaneously. Affected dogs may stand in a
" hunched up" stance or refuse to stand up
at all. They may have a fever, but this is
not consistently present. They usually have
painful swellings around the lower joints on
the legs. Some puppies will die from this
disease, some suffer permanent disability,
but many recover later. The disease is so
painful that many owners elect to euthanize
the puppy rather than watch it suffer,
despite the reasonable good chance of
recovery, long term affected dogs may be so
ill they refuse to eat. X-rays confirm the
diagnosis in most cases. There are typical
x-ray changes although it can look a little
like bone infection from a septic condition.
There is some evidence at this point that
viral or bacterial infections may underlie
some cases of HOD as canine distemper virus
has been found in the affected areas in some
dogs. There can be high white blood cell
counts and the alkaline phosphatase level in
the blood stream is often elevated. ( Konrad
had all of the above, swelling to all his
leg joints, at some very bad periods he
could not stand at all & at these times
refused to eat, he cried constantly with
pain at these times).
"There is also a theory that this condition
may occur with excessive dietary levels of
calcium or protein".
Treatment normally consists of analgesic
medications such as aspirin or Rimadyl.
Since a viral or bacterial agent may be
involved in this problem the use of
corticosteroids is questionable. Many people
try switching to a diet that is lower in
calcium ( large breed puppy food is a good
choice, before these were available people
fed adult food, but these didnt always
result in lower total calcium in the diet).
Even more potent pain relief medications may
be indicated in some puppies. Hydrocodone &
aspirin may be a more effective combination
than either one alone. Antibiotics are often
given with this condition. There is a
persistent rumour that Vitamin C
supplementation is beneficial in dogs with
HOD, this appears to be a false rumour &
there is some evidence that Vitamin C may
actually promote abnormal calcification in
these puppies. It is not a good idea to
supplement with Vitamin C.
Konrads Treatment consisted of large doses
of antibiotics over a 3 week period as
everytime he went down hill it always
started with a very high fever, he was also
given rymadyl for about a week plus steroids
20mgs everyday, with this treatment he
started to recover well, so we started to
reduce the steroids to 10mgs everyday after
about 2 months we reduced to every other day
after 10 days of this he got a fever again
Temp 41.0, so he was given antibiotics again
& 20mgs a day of steroids. We continued once
he recovered again to reducing the steroids
but still giving everyday, meanwhile Konrad
was growing not much in height but at 10
months he weighs 30kg & was having 5mgs a
day of steroids. ( he was being fed on large
breed puppy food from weaning )
3 weeks ago i reduced to 5mgs every other
day, then last week every 2 days all was
going well, he went to the Vet as a large
Heamatoma came up on his elbow, so the vet
drained it & gave him an antibiotic
injection on Friday, by Tuesday Konrad
looked unwell with a very high fever again
we rushed him to the vet were he was given
another Antibiotic injection & tablets for 3
days plus back to 10 mgs a day of steroids.
So far so good.
We will continue to try to wean Konrad from
the steroids & hope that as he grows ( he is
now almost 11 months old ) we will succeed,
but for now he is a very happy little dog,
who runs & plays with all the other dogs, &
he will stay here with us for the rest of
his life. A show dog he isnt, but we love
him dearly & is affectionately known as my
"mini Dobe" & i hope now after you have read
this, if you are lucky enough to meet Konrad,
you dont turn round & say, (just because he
is not a perfect specimen) "oh my god whats
that" because its very upsetting when you
have been through what we have with this
little man, at the end of the day he is
lucky to be alive.
A common inherited bleeding disorder. Clotting is a
complex mechanism. In addition to platelets, clot
formation is the result of a long chain of chemical
reactions carried out by individual molecules called
'clotting factors.' Each factor is numbered such
that factor I leads to a reaction with factor II
forming a new substance. This then reacts with
factor III and so on to factor XII.
In Von Willebrand's Disease, the dog
is missing a substance, which helps the platelets
form clots and stabilises Factor VIII in the
clotting process. This substance is called 'Von
Willebrand's factor.' Because of the deficient
clotting of blood, dogs with Von Willebrand's
disease have excessive bleeding upon injury. This
would be similar to haemophilia in humans.
Certain breeds have a higher
incidence of vWD than others. German Shepherds,
Dobermanns , Shetland Sheepdogs, Chesapeake Bay
Retrievers, German Shorthaired Pointers, Golden
Retrievers, Standard Poodles, and Scottish Terriers
all have a higher than normal incidence, showing
that it can be inherited.
What are the symptoms?
Excessive bleeding is the main
symptom. Bleeding generally occurs after a wound or
surgery. In these cases, the blood simply does not
clot in the normal time, and bleeding is extensive.
Dog's with Von Willebrand's disease may also develop
nosebleeds, or bleeding from the gums. Bleeding may
also occur in the stomach or intestine in which case
the stool may either have blood in it, or be black
and tarry. Some dogs will have blood in their urine.
Bleeding into the joints also occurs, which can
cause symptoms similar to those of arthritis.
The diagnosis of Von Willebrand's is
made through a simple test, which checks for the
level of Von Willebrand's factor in the blood.
What are the risks?
These dogs, without treatment, can
bleed to death following surgery, or what might be
normally considered less than life threatening
What is the management?
Transfusions with blood collected
from normal dogs is the only proven way to treat Von
Willebrand's disease. Some dogs with Von
Willebrand's disease also are hypothyroid - meaning
they have lower than normal levels of thyroid
hormone. These dogs will benefit from thyroid
hormone replacement therapy.
Some studies have been done which
suggest a drug called desmopressin acetate (DDAVP)
may help dogs with a bleeding episode. The drug can
be administered intranasally (into the nose) to
increase clotting. There is still some controversy
over whether this treatment is effective.
There is no cure for Von
Willebrand's disease. Prevention through eliminating
affected individuals from any breeding program is
the goal of veterinary medicine today. Tests are
available to determine which dogs may have this
trait. All individuals with a history of this
disorder in their backgrounds should be tested.
The Dobermann breeder and owner
should view VWD as a significant health risk, and a
fault, and strive to get rid of the mutated gene.
Test results will come back as
"clear," "carrier," or "affected." 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 realise 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 Dobermanns
(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? Firstly, you should be breeding
clear to clear producing only clear puppies,
secondly clear to carrier producing 50/50. Over
time, as the frequency of clear dogs increases, it
should be possible to breed mostly clear.
The results of breeding carrier to
carrier, (not advised & now not necessary, due to
the large genepool of clear dogs thanks to the DNA
test). This type of mating will produce 25% clear,
50% carrier, and 25% affected, on average. All the
puppies should be tested and the affected puppies
not used for breeding.
Breeding carrier to affected and
affected to affected is totally irresponsible &
In summary, responsible Dobermann
breeders are now in the advantageous position of
being able to eliminate one of the significant
diseases in our breed, 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 all
Dobermann breeders to get their breeding stock
tested, so that we can get on with eliminating this
Caused by a malformation of the
vertebrae within the neck. The spinal canal is the
tunnel within the vertebrae in which the spinal cord
lies. In affected dogs, this opening is smaller than
normal, causing pressure on the spinal cord. This
prevents neural impulses from passing through the
spinal cord. Additionally, as the animal matures,
the space within the vertebrae continues to shrink
in relation to the size of the spinal cord.
Instability between the individual neck vertebrae is
generally noted in addition to the narrowing of the
spinal canal. While any breed can be affected, over
80 percent of all cases reported are in Great Danes
and Doberman Pinschers. Genetics definitely play a
What are the symptoms?
Usually symptoms appear before four
years of age, and on average, earlier in Great Danes
than in Dobermans. An unwillingness to bend the neck
is usually the first sign, followed by weakness and
lack of co-ordination in the rear limbs, progressing
to weakness in the front limbs as well.
What are the risks?
This condition is always serious and
can progress to complete paralysis A veterinary
examination should be performed at once in animals
of these breeds showing the above signs.
What is the management?
Anti-inflammatory medications can
provide relief, but they do not correct the abnormal
spinal canal within the vertebrae. Surgery can be
performed to stabilise the vertebrae and/or to
remove a portion of the vertebrae, thus allowing
more room for the spinal cord. A full recovery is
not always achieved.
Caused by looseness in the hip
joint. The looseness creates abnormal wear and
erosion of the joint and as a result pain and
arthritis develops. The disease process is fairly
straightforward; the controversy starts when we try
to determine what predisposes animals to contract
the disease. Almost all researchers agree that there
is a genetic link involved. If a parent has hip
dysplasia, then the offspring are at greater risk
for developing hip dysplasia. Some researchers feel
that genetics are the only factor involved, where
others feel that genetics contribute less than 25%
to the development of the disease. The truth
probably lies in the middle. If there are no
carriers of hip dysplasia in a dog's lineage, then
it will not contract the disease. If there are
genetic carriers, then it may contract the disease.
We can greatly reduce the incidence of hip dysplasia
through selective breeding. We can also increase the
incidence through selectively breeding. We cannot,
however, completely reproduce the disease through
selective breeding. In other words, if you breed two
dysplastic dogs, the offspring are much more likely
to develop the disease but will not all have the
same level of symptoms or even necessarily show any
symptoms. The offspring from these dogs will,
however, be carriers and the disease may show up in
their offspring in later generations. This is why it
can be difficult to eradicate the disease from a
breed or specific line.
Nutrition: Experimentally, we can
increase the severity of the disease in genetically
susceptible animals in a number of ways. One of them
is through obesity. It stands to reason that
carrying around extra weight will exacerbate
degeneration of the joint in a dog with a loose hip.
Overweight dogs are therefore at a much higher risk.
Another factor that may increase the incidence is
rapid growth in a puppy during the ages from three
to ten months. Experimentally, the incidence has
been increased in genetically susceptible dogs when
they are given free choice high protein and high
Exercise: Exercise may be another
risk factor. It appears that dogs that are
genetically susceptible to the disease may have an
increased incidence of disease if they
over-exercised at a young age. But at the same time,
we know that dogs with large and prominent leg
muscle mass are less likely to contract the disease
than dogs with small muscle mass. So exercising and
maintaining good muscle mass may actually decrease
the incidence of the disease. Moderate exercise that
strengthens the gluteal muscles, such as running and
swimming, is probably a good idea. Whereas,
activities that apply a lot of force to the joint
are contraindicated. An example would be jumping
activities such as playing Frisbee.
5. Dilated Cardiomyopathy
Dilated cardiomyopathy (DCM) is an
inherited, irreversible heart muscle disorder that
DCM can cause ventricular arrhythmia, or erratic
heartbeats, and sudden death. Normal heartbeats are
interrupted by rapid beats that fire too closely
together, subsequently shorting out the heart, and
the dog faints. About one-third of these dogs have
no prior signs of the disease until they die. Some
dogs recover, yet some die suddenly.
Dobermanns with DCM can also develop congestive
heart failure when the heart dilates to compensate
for the weakened heart muscle. This causes the heart
to hold a greater volume of blood, while its thinned
walls continue to weaken, fluid may back up in the
dogís heart, lungs and abdomen, signs of pulmonary
oedema include coughing, rapid breathing and
lethargy. By the time the characteristic clinical
signs, such as weakness, lethargy and coughing
appear, the disease may be advanced and the
prognosis grim, therefore testing early is always
advised and if symptoms are found medication can be
given to prolong your dogs life.
DCM in Dobermanns is a challenging disease. The
biggest problem with DCM is that at this point in
time we do not fully understand its inheritance, and
more often than not it appears later in a dogs life
(7+). A dog could have been bred from numerous times
at this age and passed this problem on without
anyone knowing. Contrary to what some people say or
what you might read on the internet it is in every
line, you will find dogs in every pedigree that have
died from DCM or siblings of those dogs. As breeders
if we were to dismiss every one of these dogs you
would eliminate the Dobermann entirely! So what we
do is try to avoid what we know are problem dogs,
avoid having these dogs appearing 2-3 times in first
4 generations and test all breeding dogs.
At Wot a Thriller all breeding dogs are tested as a
minimum yearly and all females are tested
immediately before each mating as the test results
are only as good as day they are done. We like to do
it as close to breeding as possible. We start
testing all our dogs from around 18 months and we
continue to test our breeding dogs into their older
years when breeding is finished as we feel we owe it
to the progeny they have produced. We test by
echocardiogram which examines the structure of the
heart and detects functional abnormalities. We feel
this is the most accurate test we can undertake. If
advised by the Cardiologist we will also do a 24
hour Holter monitor which provides information about
the heartís electrical activity over an entire day.
As we are located in rural countryside there are no
holter monitors available to us. As we feel it is
better to routinely do both examinations, in 2018 we
will be purchasing our own Holter monitor, but
obviously if our Cardiologist in the mean time
advises us that any of our dogs need it, we will
make the 250km drive.
There are currently 4 other tests that can be done:-
Firstly Kate Meurs gene tests - testing for one of
each copy of the gene known to be a causation factor
in DCM. The tests are commonly known as DCM1 and
Troponin I high sensitivity blood test
This blood test can be used to provide an early
indication of heart muscle cell damage which occurs
in Dobermanns with cardiac arrhythmias as well as
echo evidence of DCM Normal range is 0.07 and below.
NT-Pro BNP blood test
This blood test can be used to provide early
indication of heart muscle wall stress so it's
likely to be high in Dobermanns with abnormal
echocardiograms and early DCM. Levels are very high
in Dobermanns with heart failure and symptomatic DCM.
Normal range is 750 and below.