Doberman Health Problems...Continued


  1. CVI, Wobblers

  2. CholangioHepatitis

  3. Chronic Active Hepatitis

  4. Thyroid Disease

  5. Autoimmune Hemolytic AnemiaClick Here

Some information on CVI...Wobblers...

This article was given to me by Inge Craik , with the permission from her very dear friend and Veterinarin Karen Hedberg who is very active in many aspects of Doberman disease in Australia!...Some notes have also been added and numbered at the bottom of the article, from Veterinary Internal Medicine...Ettinger,.1983 that I received from my vet!

Wobbler Syndrome - in large breeds of dogs. (Caudal Cervical Vertebral Malformation and Malarticulation) (Caudal Cervical Spondylopathy and Myelopathy)
This article is not for reproduction by any organisation and/or publication and /or private person in any shape or form without written permission.
With the kind permission, by Veterinarian, Dr. Karen Hedberg BVSc. Australia and reproduced by Inge Craik, Australia, URL:

Breeds affected: - Dobermanns and Great Danes primarily - young Danes more commonly affected. Dobermanns - young and old, can grow through the problem as youngsters, more commonly seen in middle aged to older Dobermanns (3 to 9 years of age) Other breeds who have a similar if not identical syndrome described include the Boxer, Basset, Bull Mastiff, St Bernard, Weimeraner, Labrador Retriever, German Shepherd, Rhodesian Ridgeback, Dalmation, Samoyed, Old English Sheepdog, Irish Setter, and the Borzoi. Males are affected more often, in a ratio of 2:1

(See Note #1)

Vertebral instability, either alone or in combination with vertebral malformation and/or soft tissue stenosis has been suggested as an initiating cause of spinal cord compression and associated neurologic abnormalities (VanGundy 1988 - Dobes).

Etiology (causative factors) - still obscure and include - genetics, rapid growth, nutrition. The high incidence in certain breeds suggests heredity is a contributing factor.

Structural Aspects - combined bone and soft tissue lesions (spinal cord compression) at C6-C7 and C5-C6 are most commonly seen, however C4-C5, and C3-C4 can be affected.

Malarticulation - allowing ventral displacement. This can be stable or unstable - the unstable cases are often only visible on flexed lateral views (Spondylolisthesis).

Malformation - changes can be secondary to malarticulation; the cranial edge of the vertebral foramen may be stenotic with or without deformities of the vertebral body. Arthritic changes, interbvertebral disc degeneration and collapse, disc protrusion etc. can occur in various combinations in older dogs. Most dogs have a combination of both malarticulation and malformation.

Destruction of Neurons - in severe cases, neurons are destroyed at the site of injury, usually at C6 and C7 spinal cord segments. Milder cases myelin may be lost at the site of injury, causing some loss of function that can be repaired over time if the lesion is stabilised.

Clinical Signs - vary widely. Seen as early as 2-4 months of age and as late as 8-9 years of age.

Neurologic dysfunction (signs visible) are due to the spinal cord compression exhibited in that dog. Most commonly seen in the younger dogs is hindquarter incoordination, wide based exaggerated movement and proprio-receptive deficits (stumbling, scrapping of toes). Frequent turning will often cause the dog to fall over in the hindquarters. Front legs are usually less affected than the hind-limbs, but affected dogs may have a restricted action, the limbs appearing rigid.

Rate of progression is variable according to the severity of spinal cord compression and the extent of instability and damage.

Young Dogs - especially Great Danes (less than 2 years of age), frequently have dorsal spinal cord compression due to elongation of the cranial aspect of the dorsal arch of the affected vertebrae. Dobes, Danes may be 6 months or younger when initial signs are noticed. Bull Mastiffs are generally less than 1 year of age. Affected Bassets are male, generally less than 6 months of age and have a malformation of C3.

These dogs frequently have severe ventral spinal cord compression secondary to collapse of theintervertebral disc and proliferation of fibrous tissue around the unstable area.

Older dogs often exhibit pain on movement of the neck, particularly during flexion. Signs can be as mild as neck pain to tetraplegia (paralysis of all 4 limbs).

Diagnosis - When studying this disorder it must be determined that a neurological disorder exists and not one of several skeletal diseases that occur in young dogs including OCD, HD, HOD. Most of these disorders are asymetrical, the gait appears stiff and pain can be palpated in affected joints or limbs. Neurological cases with cervical lesions have poor control over the position of the limbs, hence the wide based stance, stumbling and proprio-receptive deficits (righting relaxes of the feet).

(See Note #2

##Disorders such as congestive cardiomyopathy or hypothyroidism are frequently diagnosed in the Great Dane and the Dobermann. TSH testing is recommended in any Dobermann Pinscher with clinical signs consistent with cervical spondylonyelopathy. Supplementation of hypothyroid dogs with T4 products is recommended, and in some dogs may result in dramatic clinical improvement. (Ettinger 1989) Hypothyroid neuromuscular dysfunction symptoms include - weakness, stiffness, reluctance to move knuckling or dragging of the feet with excessive wear of the dorsal surface of the toenails and muscle wasting.

###OCD of the cervical vertebral articular surfaces of young Great Danes may be a causative factor of cervical vertebral instability in this breed. Lesions seen were similar to those seen in Cervical Osteochondrosis in swine (Olssen 1980).

Plain radiographs are useful for a rough diagnosis if there is vertebral malformation, however a myelogram is necessary for positive confirmation of the areas of spinal cord affected by compression. Apparent "tipping of vertebrae", or coning of the vertebral canal can be enormously misleading in demonstrating the involved vertebral interspaces. Without myelograms, accurate and complete diagnosis cannot be made. If surgery is needed, myelegrams are essential in the selection of the most appropriate surgical techniques that will stabilise the neck and allow the surgeon to assess the long term prospects of the affected dog.

Treatment - depends on several factors - severity of the symptoms, age, suddeness of onset, long term prospects.

Conservative - rest and cortiocosteriods are most effective in many cases. Surgery is advocated where response to corticosteroids is poor and clinical signs and/or the radiographic signs are severe. Younger dogs are often treated this way initially, however if signs persist, surgical intervention is necessary if long term improvement is to be gained. Occasionally a young dog may grow out of their problem by enlarging their verterbal canal sufficiently to accommodate the spinal cord. Older dogs, where the pain is readily controlled with rest and medication, can often be managed on long term cortico-steroid therapy. Now there are other alternatives available, such as Neck Wraps, Gold Bead Implantation and Accupuncture, which may work on some dogs verses surgery, Every Avenue is worth looking into!

Surgical - rule of thumb on this type of treatment is based on the age of the dog i.e.. if 6-8 years- surgery is probably of benefit. A 10 year dog may be better managed on tablets. Numerous methods are described and can vary depending on the cause and site of compression - plates, dorsal and ventral laminectory, vertabral body screws etc. Treatment is aimed at stabilisation and decompression of the effected section of the spinal cord. Neurological deterioration can occur subsequent to surgery (months or years later) due to invovement of an adjacent disc space. Prognosis - of affected dogs is as varied as their vertabral column lesions and neurological deficits. In general the more severe the neurological dysfunction, the less favourable the prognosis. Post surgical improvement depends on the elimination of further injury to the spinal cord and remyelination of the damaged nerve tissue.

Genetics - A simple recessive mode has been suggested in the Great Dane and Dobermann. Higher incidents are seen in males. An autosomal recessive mode for the Borzoi (generally affects older adults) has also been suggested. However there appears to be a gender influence as well (females are primarily affected in the Borzoi).

References: Veterinary Neuroanatomy and Clinical Neurology, De Lahunta 1983 Textbook of Small Animal Surgery, Newton & Nunamaker 1985 Current Techniques in Small Animal Surgery, Bojrab 1983 Textbook of Veterinary Internal Medicine, Ettinger 1989 Canine and Feline Endocrinology and Reproduction, Feldman and Nelson 1987

(Note #1)

This syndrome has also been called the wobbler syndrome, cervical vertebral instability, and cervical spondylolisthesis. The term Wobbler describes a nonspecific clinical picture, and the terms instability and spondylolisthesis do not accurately reflect the complexity of the syndrome nor the fact that instability is often not demonstrable. The name cervical spondylopathy more accurately reflects the complexity of the syndrome and therefore has become widely accepted.

The outstanding clinical feature is a slowly progressive upper motor neuron paraparesis and incoordination. Cervical pain may or may not be present. The neurologic deficit in the thoracic limbs is usually minimal and occassionally nondetectable. The reason the pelvic limbs seem more affected than the thoracic limbs is unknown, but deLahunta (1977) suggests that the more superficial position of the pelvic limb spinocerebellar tracts in the spinal cord at the site of the compression may be the reason. He also suggests that the further distance of the pelvic limbs from the center of gravity of the animal may be important.

Although the spinal cord compression is usually in the caudal cervical area (area of lower motor neuron supply to the forelegs), upper motor neuron signs predominate in the forelegs. This finding reflects the fact that chronic spinal cord compression affects the white matter more severely than the gray matter. In some cases there is a lower motor neuron involvement, usually expressed as bilateral atrophy of the scapular muscles. The foreleg gait observed in many cases is quite characteristic. The forelegs appear somewhat rigid and the stride is short , choppy , and rolling. With greater degrees of compression the thoracic limb gait resembles the pelvic limb gait, that is, paretic and incoordinated. Occasionally the onset of signs is acute, and the dog is quadriplegic when presented to the clinician.

Note #2

Diagnosis...Breed, age and clinical signs suggest the diagnosis of cervical spondylopathy, which is confirmed radiographically. Changes seen on noncontrast radiographs may consist of (1) change in shape of the vertebral body with apparent loss of the cranioventral corner of the vertebral body. (2) abnormal width and shape of the disc space cranial to the vetebral body defect. (3) calcification of the affected disc, (4) reactive osteophyte formation and end-plate sclerosis resulting from the instability of affected disc, (5) malformation of the articular processes. Myelography is required to identiy the nature and precise location of extra-dural soft-tissue masses: disc hernation, thickening of the ligamentum flavum and joint capsule, or thickening of the dorsal longitudinal ligament. The use of a hyperextended lateral projection is of great value in demonstrating the maximum degree of cord compression.

Note #3

I would like to add, that some dogs have been treated with accupuncture by a Licensed veterinary accupuncturist, with some great success, this is another avenue to seriously check out!

More Links to Wobblers (CVI) Information!

Wobblers Syndrome Information
Wobblers Syndrome, related to Great Danes!
Neck Wrap Info for Wobblers!
A Group on Yahoo to join Regarding Wobblers Syndrome...
Another bit of information on Wobbler
Doberman Neckwrap done on Sylvia...
Another information Page on Wobblers...
An Article on Food and antioxidents in realation to many diseases is dogs, I dont know if this is true or not. Its basically a add with information.
Health Information Links, Including Wobblers.
Gold Bead Implant information, regarding Wobblers!



This is the disease Jamie very recently got critically ill from, its a bacterial disease of the liver, all dogs have bacteria in their liver, but Jamies got out of hand. The Doctors told me, that they were not sure what it came from, but it could have been from Jamies' heart not pumping blood fast enough thru-out his system and liver, as Jamie has Cardiomyopathy, and the bacteria could have backed up and multiplyed and caused the inflamation of the liver, thus causing swelling and closing off the bile ducts and backing up the bile in the liver...The onset was very sudden, it started with Jamie vomiting, and within four hours he kept vomiting and got very weak and lethargic and depressed, also started to dehydrate...He started with a 102.3 fever which escalated to 105.1 and then stayed around 103.8 or 104 for a few days. He had very aggresive IV therapy with antibiotics, fluids, nurishment, and he had ultrasounds and liver biopsy also...He was very sick and his blood chemisty was going astray and there were days when he was not expected to make it...He was very sick with this for an entire explanation and possible cause of the disease are below:


Cholangitis, inflammation of the intrahepatic biliary ducts, has been reported cats and dogs. May be associated with secondary inflammation of the surrounding hepatic parenchyma, and termed cholangiohepatitis. Dx is made on the basis of clinical signs (which may wax and wane), liver biopsy, anaerobic and aerobic cultures of bile and hepatic tissue, and rule-out of other causes. Lesions at biopsy can show suppurative, chronic-nonsuppurative, or cirrhotic lesions. There is usually increased activity of ALP and GGT, conjugated hyperbilirubinemia, and hyperglobulinemia. In the anicteric cat the two-hour postprandial bile acid concentration is usually abnormal. Mild nonregenerative anemia and a neutrophilia with a mild left shift are sometimes seen. Treatment was discussed by Day, by Jackson et al. and by Forrester et al.

Species:Feline, Canine


Anorexia, Dehydration , Diarrhea , Dullness, Excessive salivation, Fever, Hepatosplenomegaly, Icterus, Internal abdominal mass, Pain on external abdominal pressure, Pale, Polydipsia, Underweight, Vomiting or regurgitation, Weight loss


GAGNE JM ET AL. histopathologic evaluation of feline inflammatory liver disease. vet pathol 1996;33:521-52

WEISS DJ ET AL. relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats. javma 1996;209:1114-1116

DAY DG. feline cholangiohepatitis complex. vet clin n a: small anim pract 1995;25:375-385\

JACKSON MW ET AL. administration of vancomycin for treatment of ascending bacterial cholangiohepatitis in a cat. javma 1994;204:602-605.

FORRESTER SD ET AL. cholangiohepatitis in a dog. javma 1992;201:1704-1706.

62 Possible Diagnoses of vomiting and jaundice in dogs

o Aflatoxin toxicity, aflatoxicosis in dogs
o Amyloidosis in the dog and cat
o Autoimmune, immune-mediated, hemolytic anemia in dogs and cats
o Babesiosis in the dog and cat
o Bacillus piliformis (tyzzer's disease) in the dog and cat
o Bile duct obstruction in dogs and cats
o Blood transfusion reaction in dogs and cats
o Canine adenovirus, infectious hepatitis or 'blue eye'
o Canine ehrlichiosis, ehrlichia canis
o Canine leishmaniasis
o Canine parvovirus-2, parvoviral enteritis
o Canine salmonellosis, salmonella in dogs
o Cholangitis, cholangiohepatitis in cats and dogs
o Cholecystitis, cholelithiasis, choledocholithiasis
o Chronic inactive, persistent, or active hepatitis in dogs
o Copper toxicity in bedlington terriers and other breeds
o Cycad, zamia, cycas, poisoning in dogs
o Destructive cholangitis in dogs
o Diabetes mellitus in the dog and cat
o Diabetic ketoacidosis in dogs and cats
o Diaphragmatic hernia, rupture, in the dog, cat, and pig
o Drug-induced canine hepatic disease
o Gastric neoplasia, stomach cancer, in dogs and cats
o Heartworm, dirofilaria in dogs and cats, angiostrongylus in dogs
o Hemangiosarcoma in the dog and cat
o Hemobartonellosis in cats and dogs
o Hepatic encephalopathy in dogs and cats
o Hepatic fibrosis, cirrhosis, of the canine or feline liver
o Hepatic necrosis, 'toxic hepatopathy', in cats and dogs
o Hepatotoxicity in dogs fed meat contaminated with indospicine - exotic
o Heterobilharzia americana, canine schistosomiasis
o Histoplasmosis in dogs and cats, geotrichosis in dogs
o Hypoglycemia-ketonemia, pregnancy toxemia in dogs
o Intestinal, cecal, colonic, rectal neoplasia in dogs and cats
o Leptospirosis in dogs and cats
o Liver, hepatic, abscess in dogs and cats
o Liver, hepatic, hepatobiliary neoplasia in dogs
o Lymphoid or myelogenous leukemia in dogs and cats
o Lymphosarcoma, malignant lymphoma in dogs
o Malignant histiocytosis, histiocytic medullary reticulosis, dogs and cats
o Mushroom poisoning in dogs, cats and pigs
o Mycobacterial infections in dogs and cats, tuberculosis
o Myeloproliferative disease in dogs and cats
o Neoplasia of the exocrine pancreas in dogs
o Nonsteroidal anti-inflammatory drug toxicity in dogs
o Pancreatitis, pancreatic abscess, in dogs and cats
o Phosphorus toxicity
o Poisoning in dogs attributed to blue-green algae
o Portocaval, portosystemic shunt in dogs and cats, venous anomalies
o Rocky mountain spotted fever, rickettsia rickettsii, in dogs
o Rupture of the canine or feline gallbladder or bile duct
o Snake bites, snakebites
o Splenic neoplasia, tumors of the spleen, in dogs
o Stomatitis-hypertrophic gastritis in drentse patrijshond dogs
o Superficial necrolytic migratory erythema, dermatitis, in dogs
o Torsion of the spleen, splenic pedicle, in dogs
o Toxoplasmosis in the dog
o Trypanosomiasis in dogs - exotic
o Tularemia, francisella tularensis in cats and dogs
o Yersiniosis in dogs and cats
o Zinc toxicity in the dog
o Zygomycosis, pythiosis, in dogs and cats



By Mervi Ihantola


Chronic active hepatitis (CAH) is a yet relatively unknown liver disease
with dramatical consequences for the Dobermann. The disease was first
discovered by us in Finland at the end of the 70s. Articles in medical
journals began appearing in the beginning of the 80s in the USA. As
there is too much copper in the liver, the condition has been also called
copper toxicosis. Other names used for CAH are chronic hepatitis and
doberman hepatitis. The symptoms are so typical of CAH patients that
they caught the eyes of the Finnish Dobermann breeders in the 80s.
This led to the beginning of an erradication program. This disease is
recognized worldwide as data has been published at least in USA,
Finland, Holland, Sweden, Germany, England, Australia.


The disease is most likely to affect a female aged four to six years.
Males develop CAH more seldomly. The initial symptom, though often
neglected, is polydipsia (heavy drinking). The dog may eat a lot of snow
during the winter and tends to seek some other sources of water,
besides its own cup. Heavy drinking may only be temporary or
intermittant. When the condition progresses further, a poor apetite
vomiting and weight loss soon follow. As the disease advances, the
mucous membranes start to turn yellowish. This is most apparent in the
eyeballs (sclera), the gums and on the skin in areas where hair is scarce
such as the ears and the inguinal region. This stage is called icterus and
is typical of any liver condition.because bilirubins (bile pigments)
accumulate in the blood stream and tissues due to the liver dysfunction.
Weight loss becomes accelerated and the dog develops free fluids in
the abdomen, often so much that it looks like a puppy that has just
eaten a huge dinner. The only differences in the appearance are the
pronounced ribs and spine. The dog is tired and lethargic, although not
entirely incapable of running and playing if required, as Dobermanns
always like to do.


The Finnnish Kennel Club supported the start of a wide based
collection of blood samples from healhy Dobermann females in 1987.
We anticipated to find changes in liver enzymes like ALT (s-ALT) from
normal dogs before the onset of clinical signs. The suspicions proved to
be valid. The serum ALT values were clearly elevated for a long time
before the individual itself showed any signs of the disease. As a matter
of fact, as the project has continued we have noticed that some dogs
with elevated liver enzyme values may develop the clinical signs quite
late. Only the elevated liver enzymes indicate the presence of problems
in the function of the liver. The right nutrition among other yet unknown
reasons is believed to play an important role in keeping the individual
from developing symptoms. This is not surprising considering the
responsibility the liver takes in metabolism; it becomes over loaded with
the wrong nutritions.


In Finland, we want to discover the sick animals long before the
problems show up. During the years we have collected blood samples
from dogs that do not present any signs of the disease. A majority of
the test are normal of course continuously. The ideal procedure is to
start investigations at the age of two to three years and continue yearly
or every two years up to the age of about seven years. Nowadays
CAH testings are official and obligatory for Dobermanns which are
used for breeding. To get puppies registered, both parents must have
results no more than ten months old at the time of the mating.

Every now and then we discover individuals with abnormal values.
Many of them are just innocent, once in a life time jumps, but few of
those elevated values remain high. These are the dogs that should be to
followed by blood tests. The definitive diagnosis of CAH is made only
by biopsies taken from the liver. That is recommended for individuals
with high ALT values for two to three consecutive tests or several high
peaks during one year. We are able to detect any deterioration at their
health condition by following the test values. Those Dobermanns with
ALT values over the normal laboratory range (VETLAB, Tampere; the
normal range is 24 - 136 U/I ) more than once, are also controlled for
SAP, bilirubin, bile acids, and if needed, other blood parameters to get
more information about the situation and to know more about the
prognosis. Different laboratories have different normal ranges for ALT.
In order to obtain reliable and compareble results, qualified lab is
needed. In Finland, we approve only one lab for official tests by Finnish
Dobermann Club / Finnish Kennel Club.


What if the dog gets the clinical signs? Then the situation is worse.
Blood tests may show s-ALT to be five to ten times over the normal.
Other blood parameters are often not good either. At the moment we
do not know the cause of the disease and it is very difficult to try to
cure CAH with specific treatment. We have to try the medicines which
relieve the symptoms. Initially, drugs which chelated the copper
(D-penicillamine) were used. This didn't seem very encouraging. It
would seem that copper is not the reason for the liver damage, as is the
case in Bedlington hepatitis. Copper appears only secondary and not in
the excessive amounts of Bedlington. The most valuable medicine is still
corticosteroids. On the other hand, steroids and the Dobermann is not a
good combination and the use of this medicine can result in some
problems. It seems that the breed is sensitive to its use. Corticosteroids
often results in side effects which we would prefer to avoid. The
treatment of clinically ill dogs demands a lot of precision and caution.
With the proper treatment, it is possible to ease the progress of CAH
and prolong the inevitable a little further. The difference between the
beginning of the symptoms and the start of the treatment makes a great
difference in survival time. According to our statistics, the survival time
can be from some weeks to several years. New medicines to treat
patients with CAH are continuously being researched, but until this day
we do not have many promising alternatives. We prefer a strict diet
based on home-made food low in copper and abandoning all comercial
preparations. The food regiment is the same for dogs with no clinical


Just by controlling all breeding stock, the number of CAH cases seems
to be decreasing. We had great difficulties in the 80s just before our
quarantine system for dogs was abandoned. Most individuals were
related to some heavy used carriers of CAH. In 1988 and onwards we
were able to import many new dobermann lines. It seemed to help a lot.
Or perhaps the problem is just hidden by some of the owners and
breeders? Anyway it is almost impossible to breed with individuals with
high ALT results nowadays in Finland. Not because it is not allowed
(because it is, only test has to be made), but mostly because the results
are public. Public opinion is important in selling the puppies. We are not
free from CAH. Our first recognized cases to Finland came with the
imported animals from Germany. We have still found many individuals
with CAH to have direct ancestors of imports or are imported
themselves. So it is not possible to stand against CAH alone. It is sad
that we are dependent on European breeding stock, which is totally out
of control with CAH. That is of course mainly because breeders and
veterinarians are not aware of the problem called CAH. The problem
can come more common again in Finland, but also elsewhere due to
two reasons. We sometime use some males heavily all over Europe not
knowing their health state and population number can drop quickly in
the near future because of the ear and tail cropping legislations, leading
to serious genetical problems .

Another Page on CAH


Thyroid Disease

Jan Cooper

This small gland is a hormone producer that affects many parts of the body.
When certain diseases or ailments are suspected in a dog, testing for a
thyrod imbalance can often lead to a more accurate diagnosis and better
treatment. The little thyroid is more often than not one of the guilty
culprits. Edward Baker, VMD, refers to the thyroid as the body's chief

This important little gland consists of two oval bodies located in either
side of the neck. There are also tiny parts of thyroid tissue in other
areas of the chest and even around the heart.
There are two (2) forms of thyroid hormone secreted by the thyroid gland;
T3 (triiodothyronine) and T4 (thyroxine). T3 is usable thyroid hormone
while T4 must first pass through the liver and other tissues before it can
become T3, the usable thyroid.

Here is where it begins to get a little complicated, but I'll do the best I
can to help simplify it. The thyroid gland itself is regulated by two
different hormones, TRH and TSH. Now, if T4 gets too low, (remember it's
not usable yet when it starts traveling around the body) the brain tells
the TRH, "Hey, wake up, go get TSH and tell him to get to work!" Now TRH
knows that TSH 'hangs out' at the nearby Pituitary gland, and so heads
straight there to find him. Well, as soon as TSH hears about the thyroid
shortage he races to the thyroid gland and stimulates it to get busy and
produce more thyroid hormone. Hence TSH stand for THYROID STIMULATING
HORMONE while TRH, being the first one to be released into active duty, is

As a consequence of all of this, Hypothyroidism (the shortage of usable
thyroid in the body) is usually the condition seen when a thyroid imbalance
is suspected. Hypothyroidism is becoming all too common in our breed and
all of our dogs should be tested.

Why do skin problems seem to go hand in hand with thyroid imbalance? In
order for our dogs to have healthy skin and coats, the cells that make up
the body must be healthy and multiply. It is not fully understood, but
thyroid hormone is essential in regulating the metabolism of each
individual cell. Whenever the cells cannot function efficiently, one of
the visible results is the skin will loose it's elasticity, and can
ultimately result in dry, crusty, scaly skin. The end result can be a dog
with a very sparse coat and a dull, almost hardened gray skin that will
have a obnoxious odor. A dog left untreated will be miserable with
uncontrollable itching all over and will further damage itself by chewing
to the point of producing raw and oozing sores, a setting ideal for
bacterial infections.

It is found to be a fact that hypothyroidism is definitely associated with
reduce resistance and a greater susceptibility to bacterial infections. So
if your dog develops any type of skin ailment or a wound that does not seem
to respond readily to treatment, you might want to check for a thyroid

Part 2

Hypothyroidism is becoming very prevalent in the Rottweiler.
Last month I explained how the thyroid is regulated by two different
hormones, the Sytimulating Hormone (TSH) and The Releasing Hormone (TRH).
I also explained that because of the amount of thyroid hormone a dog needs,
hypothyroidism is the disease usually seen whenever there is a thyroid
imbalance or malfunction. This month I will touch on the testing for
hypothyroidism and the importance of testing ALL of your potential breeding

There is a lot of confusion about whether a dog has thyroid disease or
not. Most people seem to think that they can tell if there is a problem
and therefore only then they should take their dog to be tested. When it
comes to the thyroid, nothing can be further from the truth.
As thyroid disease develops, it usually starts out as autoimmune
thyroiditis. ³As what?² you ask. The best way I can explain it is that
there are antithyroid antibodies in the blood. In people, this is
sometimes referred to as Hashimotoıs disease or lymphocytic thyroiditis.

The worst part of this is that in 90% of the IS genetic!
Without testing your breeding stock you wonıt know it until later when
clinical symptoms begin to appear. Tragically this may be after the
dog/bitch has been bred and then the predisposition for the disease is
passed on to the next generation....and so on....and so on.

Letıs get to the testing part, since you should now have a basic
understanding of T3 and T4. Remember, T3 (triiodothyronine) is the usable
thyroid hormone and T4 (thyroxine) has to be converted into T3? The level
of these two hormones is not always inter-related, in other words, the dog
may show adequate T4 and yet not be producing enough T3, or visa versa.
That is oversimplified, but I think you get the idea.

Most Veterinarians request only the T4 hormone level that is found in
the blood to be measured by their lab. But since there is a tiny amount of
T4 hormone that is not in the blood, or ³free T4², that is also converted
and aids intracellular health, this too should be measured.

The only way to know if your dog has thyroiditis and later
is a candidate for hypothyroidism is to be sure you ask
for a measurement of the total T3 and
T4 along with a measurement of the ³free T3 and T4². Since studies have
shown a definite link between the Cholestrol level and T4 in dogs, your
veterinarian should also request a cholestrol level from the SAME blood
samples. The results of the testing for cholestrol in relationship to T4
is called the ³K² values.

With the addition of this test, you may detect early thyroid disease
before any clinical symptoms are apparent. Once clinical symptoms appear,
the ³K² value can aid in identifying whether the dog has low, normal or
high thyroid function.
If there is no local lab that is familiar with these additional tests,
then you may wish to talk to your Veterinarian and have him contact:

P.O. BOX 30076
LANSING, MI. 48909
(517) 353-0621


mental dullness
exercise intolerance
neurologic signs
(polyneuropathy, seizures)
weight gain
cold intolerance
mood swings
stunted growth
chronic infections

bone marrow failure
low red blood cell count (anemia)
low white blood cell count
low platelaet

corneal lipid deposits
corneal ulceration
keraconjunctivitis sicca ("dry eye")
infections of eyelid gland
(meibomian gland)

laryngeal paralysis
facial paralysis
"tragic expression"
knuckling or dragging feet
muscle wasting
head tilt
drooping eyelids

dry, scaly skin and dandruff
coarse, dull coat
bilaterally symmetrical hair loss
"rat tail" or "puppy coat"
seborrhea or greasy skin
pyoderma or skin infections
chronic offensive skin odor

slow heart rate (bradycardia)
cardiac arrhythmias


infertility or either sex
lack of libido
testicular atrophy
prolonged interestrus interval
absence of heat cycles
silent heat
weak, dying or still born pups

IgA deficiency
loss of smell (dysosmia)
loss of taste
chronic, active hepatitis
adrenal indocrinopathies
pancreatic indocrinopathies
parathyroid indocrinopathies

The above list was graciously provided by W. Jean Dodds, D.V.M.
If your dog seems to suffer from any of these ailments, you may want to
discuss his/her thyroid with your veterinarian.

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More Links to Information on THYROID!

Thyroid Info!
Thyroid Disorders
More On Thyroid
Thyroid and Aggression
Thyroid and Bizarre Behavior
Thyroid and Behavior

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Cardio Update...1/22/99!

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