Medical Issues: The Dobermann: Dobermann Breed Standard :
   
 
 
Most Dobermanns in Australia live a full healthy life without any major medical complications provided they are loved, well fed, regularly groomed, nails clipped, kept free from fleas, exercised, frequently treated to remove Intestinal worms (including the Hydatid tapeworm), given regular preventative Heartworm preparations from an early age and vaccinated annually, preferably against Distemper, Parvovirus, Hepatitis, and both varieties of Kennel Cough.

Nevertheless there are some recognised medical problems in connection with the breed of which prospective owners should at least be aware. However, it must be emphasised that these problems are in the main not confined to the Dobermann breed and it should also be noted that all reputable Breeders continually strive toward the elimination of hereditary problems - both health and temperament. This section is aimed at providing a potential owner with a basic understanding of some of the medical problems which occur within the breed. Your veterinarian is the expert and the best source of more definitive information.

Consequently this is not intended to be exhaustive, but addresses those problems I have become familiar with during my reading about the breed. It will be continually updated as new information comes to hand and my own understanding increases. Some medical problems are hereditary, some environmental and others probably a combination of a number of circumstances. They include:

CERVICAL VERTEBRAL INSTABILITY
DILATED CARDIOMYOPATHY
VON WILLEBRAND'S DISEASE
LIVER DISEASE
HYPOTHYROIDISM
HIP/ELBOW DYSPLASIA
VARIOUS

CERVICAL VERTEBRAL INSTABILITY:

This is also known as Cervical Spondylopathy, Cervical Stenotic Myelopathy, "wobbler" syndrome. According to Canine Medicine and Therapeutics, Fourth Edition, Blackwell Science, 1998   this is due to "A combination of cervical (neck) vertebral malformation, increased vertebral laxity and hypertrophy of intervertebral ligaments and articular facets which causes stenosis of the vertebral canal and compression of the caudal cervical spinal cord." It "is seen in adult Dobermanns, young Great Danes and is occasionally seen in other large breeds of dogs".

Basically, the spinal cord and its nerve tracts are pushed against the roofs of the vertebrae, and the excess pressure is manifested in abnormal limb functions. Initially there may be a wide stance of the hind legs, with stumbling and lack of co-ordination; the nails and feet of the hind legs may catch or be dragged on the ground. There is often considerable difficulty in turning.

There can also be great difficulty in positioning when toileting. In more severe cases the front limbs may also be affected. Many different factors have been proposed as causes of CVI. These include long necks, heavy heads, breed conformation, fast rate of growth, over nutrition, traumatic injuries and the over eager use of choker chains. Nevertheless, there appears to be some disagreement as to whether or not heredity plays a major role. Some views are:

According to Dobermanns, An Owners Companion, Howell Book House, 1991 "The genetic basis for CVI is not clear. It is probably multifactorial, with a dependence upon hereditary, environment and husbandry. In this respect it shows similarities to the inheritance of hip dysplasia."

Conversely, according to The Australasian Dobermann, Pace Publishing, 1996 "Canine Wobbler Syndrome is a hereditary disease" as evidenced by "it's high prevalence in the

Dobermann breed and higher prevalence in some lines of Dobermanns", although "the precise mechanism by which it is passed to the next generation is yet to be determined."

On the other hand Dobermanns Today, Ringpress and Jimmy Richardson, 1995, says "The causes are not entirely clear. It has been suggested that the condition is related to breed conformation and that the position of the head and neck tends to concentrate all the biomechanical forces on the base of the neck, which is where most of the problems occur. Diet is also considered to be important. Feeding a high protein diet during the two to six months of age period, and the giving of excessive amounts of calcium, are accepted as being partly responsible for producing the condition. There may be a hereditary factor involved, but this has not yet been proven."

DILATED CARDIOMYOPATHY:
This manifests itself as either sudden heart failure or as congestive heart failure. It is only one form of cardiac disease, but is by far the most common form in Dobermanns.

According to Canine Medicine and Therapeutics, Fourth Edition, Blackwell Science, 1998, "The pronounced breed predispositions in dogs to Dilated Cardiomyopathy (DCM) suggest a hereditary component. It is characterised by impaired ventricular function and dilation of one (typically the left) or both ventricles of the heart.

When heart failure develops, the onset of clinical signs is frequently acute, and presenting signs typically include dyspnoea, cough, syncope/collapse, anorexia and weight loss, reduced exercise tolerance, lethargy, weakness, ascites (if concomitant right-heart failure), sudden death.

"There are breed differences in the presentation and progression of the disease. Dobermanns typically present with acute-onset left-sided failure, ventricular tachydysrhythmias, a short clinical course and a high incidence of sudden death. DCM is primarily a disease of young and middle-aged dogs, although a wide range of age groups may be affected. Giant and large breeds are predominantly affected, with some medium sized breeds".

"The prognosis appears to vary with the breed and the severity at presentation. Patients identified early as a result of the discovery of a dysrhythmia may remain free of clinical signs and compensated for years. Once cardiac failure develops, however, the outlook is poor. Most patients die or are euthanased within 6-12 months of the development of overt cardiac failure, although with careful management some patients will survive for years. The prognosis in the Dobermann seems particularly poor, with most patients living only 3-6 months after the development of cardiac failure." 		Other breeds specifically mentioned in this publication in relation to DCM include Boxers, Cocker and Springer Spaniels, giant breeds such as the Irish Wolfhound, St Bernard, Great Dane and Newfoundland.

Again, according to Dobermanns, An Owners Companion, Howell Book House, 1991 "The mode of inheritance is not known, but certain dogs and families of dogs seem to occur in the pedigrees of cardio-death Dobermanns.


" Dr Martin Strong BVSc in The Australasian Dobermann, Pace Publishing, 1996 postulates "that defects in metabolism leading to enzyme deficiencies necessary for heart muscle health is the cause of the disease" and that "these defects in metabolism and hence the disease are inherited in the next generation." He also includes German Shepherds amongst the breeds prone to DCM and agrees that " young to middle aged male dogs are the most common victims." 		In the USA, where Dobermanns are said to be affected with DCM more than all the other breeds combined, research funded by the Dobermann Pinscher Foundation of America and the Morris Animal Foundation to find the genetic markers and develop a DNA test for Dobermann Dilated Cardiomopathy is underway.

Until that DNA test to identify those dogs that are genetic carriers or at risk of developing the disease is available, Dr Larry P Tilley, DVM, ACVIM of VET MED FAX Consulting Services, Santa Fe, USA, is reported to believe that a simple EKG can lead to early detection, and that every Dobermann one year old and older should have an EKG evaluation annually as a routine screening procedure, with cardiac ultrasound to confirm or rule out DCM in the event that a premature ventricular contraction (PVC) is detected.

Refer article : "Dobermann Dilated Cardiomopathy, What Can Be Done Now? By C David McLasughlin, DVM, as published in The Dobermann Digest, October 1999.

VON WILLEBRANDS DISEASE:

This has been reported in at least 54 different dog breeds worldwide including Golden Retrievers, Scottish Terriers and Dobermanns. It occurs in humans as well.

It arises from abnormalities in the blood clotting system. According to Canine Medicine and Therapeutics, Fourth Edition, Blackwell Science, 1998, " severe vWD causes spontaneous haemorrhage at an early age, whereas milder forms of the disease may not be detected until an episode of vascular injury such as trauma or surgery causes excessive or prolonged haemorrhage.

Older dogs with subclinical vWD exposed to factors that impair platelet function (treatment with aspirin for example) may then develop spontaneous haemorrhage. Dogs with subclinical vWD that then develop hypothyroidism are also thought to be more susceptible to haemorrhage." "The disease is incurable, and therefore euthanasia is recommended in severely affected patients that suffer from multiple life-threatening episodes of haemorrhage at an early age.

Dogs with milder forms of vWD, however, can have a normal life expectancy if potential causes of blood loss are anticipated and avoided if possible, and if episodes of active haemorrhage are treated appropriately with transfusion and/or desmopressin."

In the past, the common clinical test for vWD was assay of plasma levels of von Willebrands Factor, a blood glycoprotein, with low levels of vWF confirming the presence of vWD. Although it was commonly understood that vWD was inherited, until recently the method of inheritance was not understood.

However, the good news is that the method of inheritance in Dobermanns HAS been identified and we now have at our disposal the means of eliminating this disease from our breed.

Research has demonstrated that vWD in Dobermanns is due to the presence of a gene mutation. The particular type of mutation found in Dobermanns has occurred in some human patients with vWD. The mutation is of a type such that completely normal vWF is made about 5-10% of the time, which explains why affected Dobermanns have a milder form of vWD than, for example, affected Scottish Terriers.

A vWD affected Dobermann has two of the mutated genes and it is believed such dogs can end up with around 10 to 20% of normal vWF in their blood. In these, providing the bleeding stress isn't too great, this 10 to 20% of normal vWF can prevent undue bleeding. However a dog with only 5% normal vWF is obviously at greater risk.

The discovery of the mutation and the development of a DNA test now provide breeders with the opportunity to get rid of the mutant gene. Available through VetGen LLC in the USA this DNA based test is definitive and final, a lifelong, permanent determination of the vWD status of each dog tested

The test classifies Dobermanns as to whether they are vWD Clear (both genes normal), Carrier (one gene mutated, themselves free from any bleeding risk but can transmit the mutant gene to their offspring) or Affected (two mutant genes) and so gives breeders the ability to predict the outcome of any mating providing they know the status of the stud dog and bitch.

Matings of Clear to Clear or Clear to Carrier will not produce any vWD Affected offspring, although in the latter case pups which are Carriers can result. A mating of Carrier to Carrier can statistically produce a percentage of vWD Affected offspring, so is not recommended. This test is available to Australian breeders through GENTEST, Mrs Inge Craik of Aciro Dobermanns, Sydney.

For further reading see "DNA Studies in Dobermann 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. Dobermann Quarterly, Winter 1996, pp301-302. 		LIVER DISEASE:

Again, from the Canine Medicine and Therapeutics, Fourth Edition, Blackwell Science, 1998 "Certain breeds are more prone to develop liver disease than others. There are also some differences in disease incidence with respect to gender and sex. For example female Dobermanns are more prone to develop liver disease than are males. Breeds predisposed to liver disease include the Bedlington Terrier, West Highland White Terrier, Dobermann, English Cocker Spaniel, American Cocker Spaniel, Skye Terrier, German Shepherd, Standard Poodle, Irish Wolfhound, Yorkshire Terrier, Maltese Terrier". "Many substances can damage the liver".

Perhaps the most widely known is copper. "Inherited copper storage Hepatitis in Bedlington Terriers is common and world-wide; a different type of copper storage hepatitis has been described in West Highland White Terriers.
Dobermanns are affected by a idiopathic chronic (active) hepatitis, in which copper accumulation is considered secondary and not primary as in copper toxicosis in the Bedlington Terrier. The majority of Dobermanns presented are females and the mean age at presentation is five years. Clinical signs are typical of liver disease with polydipsia, polyuria, weight loss, ascites, icterus, anorexia, depression, vomiting and diarrhoea. Many dogs are presented in a late stage of liver disease and the prognosis is often poor.

However, dogs diagnosed in the early stages of the disease have a favourable prognosis.

Chronic liver disease associated with copper accumulation also occurs in Skye Terriers. American reports indicate that copper accumulation may be a potential problem in many other breeds including Labrador Retrievers, Cocker Spaniels, German Shepherds, Pekingese and others.

However the role copper plays in the development of chronic liver disease in dogs is still debated."

HYPOTHYROIDISM:

This is a common disease in dogs. Canine Medicine and Therapeutics, Fourth Edition, Blackwell Science, 1998 describes it as "It affects all organ systems causing a decrease in the basal metabolic rate. The most common clinical signs are metabolic and dermatological abnormalities.

The reproductive system may also be adversely affected. Other organ systems which may be affected include the eyes, heart and peripheral and central nervous system.

Breeds suspected of a predisposition for hypothyroidism include the Golden Retriever, Dobermann, Great Dane, Shetland Sheepdog, Cocker Spaniel, Airedale, Dachshund, Irish Setter, Miniature Schnauzer, Poodle, Boxer, Pomeranian."

Thyroid Function tests are utilised to check for normal and abnormal thyroid function.

HIP/ELBOW DYSPLASIA:

These refer to an abnormality in the ball and socket joint. There can be wide variations in both the degree of the abnormality and the secondary changes that may accompany it. In very severe cases, the bone surfaces of the joint may show considerable damage.

According to Dobermanns, An Owners Companion, Howell Book House, 1991 "the heritability of hip dysplasia is approximately 30%, but varies for different breeds. The modifying factors include excesses in diet, particularly overfeeding and un-necessary supplementations, and extreme exercise when young.

X-ray techniques enable examination and a numerical grading of dogs for dysplasia. It is believed that dogs X-rayed at twelve months or more give results that are unlikely to change with time. Under twelve months of age the results obtained cannot be extrapolated reliably to later life".

It should be noted that in Dobermanns Today, Ringpress and Jimmy Richardson, 1995, the statement appears "It is rare to see a Dobermann showing any evidence of hip dysplasia, and statistics suggest that it is not such a problem with them as with many other breeds. However it would be most unwise to conclude that there is no need to be concerned."

OTHER VARIOUS MEDICAL PROBLEMS ASSOCIATED IN THE LITERATURE WITH, BUT NOT ISOLATED TO DOBERMANNS,
INCLUDE THE FOLLOWING:

* CHRONIC RENAL FAILURE
* CONGENITAL NEUTROPHIL DYSFUNCTION

*DRUG INDUCED ARTHRITIS:


Quoting from Canine Medicine and Therapeutics, Fourth Edition, Blackwell Science, 1998 "Immune based polyarthritis can be associated with the administration of certain drugs, particularly antibiotics……. Other manifestations besides polyarthritis may be seen. Eg., dermatitis, glomerulonephritis, myositis, thrombocytopenia. The dog rapidly improves (2-7 days) once the drug administration is stopped. The Dobermann is apparently predisposed to poly-arthritis associated with sulphonamide drugs".

* EXOCRINE PANCREATIC DEFICIENCY

* GASTRIC DILATION, VOLVULUS AND GASTRIC TORSION

Commonly called "bloat" is a sudden enlargement of the stomach which is usually full of fermenting food and gas. The condition is complicated when the stomach twists, blocking both the entrance from the throat and the exit to the small intestine. The dog is in great pain and distress and this is one of the true veterinary emergencies as the condition can be fatal within a very short time.

As this can be a life threatening problem, taking all possible preventative precautions is wise. Unfortunately this still does not guarantee elimination of the risk of GDV occurring.

My vet has listed the major risk factors as including: deep chested conformation, large meals (especially food that may swell after eating, eg., dry food), exercise around the time of eating, within up to two hours either pre or post the meal.

Most cases are seen around 10.00pm, some 3 to 5 hours after eating. If surgery is needed (ie., they can not be decompressed with a stomach tube), on average my vet also advises that twenty-five percent will not survive. The sooner the problem is noticed, the better the prognosis

 

* IMMUNE MEDIATED HAEMOLYTIC ANEMIA
* KERATINISATION
* LICK SORES
* PANOSTEITIS
* PERSISTENT HYPERPLASTIC PRIMARY VITREOUS
* PROGRESSIVE RETINAL ATROPHY
* PROSTATIC DISEASE
* SEASONAL FLANK ALOPECIA
* SPECIFIC IMMUNITY DEFECTS: Selective IgM deficiency
* SKELETAL SKURVY


* SULPHONAMIDE HYPERSENSITIVITY:

Quoting from Canine Medicine and Therapeutics, Fourth Edition, Blackwell Science, 1998 "Dobermanns appear to have increased risk of sulphonamide hypersensitivity, possibly due to delayed sulphonamide metabolism. Other antibacterial drug breed susceptibilities have not been reported."


In an article in Dobermann Quarterly, Fall, 1994, Robert M Brown DVM warned that "under no circumstances should you allow your veterinarian to use any of the trimethoprim-sulfa mixtures on your Dobermann for any reason." Although he did not elaborate in the article it is highly likely this sulphonamide hypersensitivity is the reason.

* ZINC DEFICIENCY