All mammals will eventually die of heart failure if they remain otherwise healthy. DCM is a progressive Dobermann heart disease causing weakening of the left ventricle and muscle walls. The left ventricle becomes dilated and has no muscle strength. There are two types of death from DCM – the first is sudden and unexplained death, the other is a prolonged death of congestive heart failure where the lungs back up with fluid, starts to cough to expel fluid from the lungs. If a Dobermann starts to cough and kennel cough is ruled out, DCM should be considered. DCM is not specific to age, but most DCM dogs successfully hide their condition which starts to be symptomatic usually from around 5 yrs onwards. There is no cure, just medication – primarily diuretics. DCM is the breed’s 3rd biggest killer after old age and cancer (just as with humans). DCM is hereditary BUT, importantly no-one knows HOW. It is an apparent paradox that short-lived dogs can produce long-lived dogs, and vice-versa. We have bred dogs in one litter with three having sudden death at 7, 8, 8.5 yrs, and three at 11 (cancer), 11.3(cancer), and 11.5 yrs (spinal collapse).

If you consider the Punnett equation would work as such:

• Where “A” is Positive/Affected and “a” is Clear/Negative:
• Aa x aa would mean offspring would each have a 50% chance of inheriting the illness.
• Aa x Aa would mean offspring would each have a 75% chance of inheriting the illness.
• AA x aa or AA x AA would mean 100% could inherit the illness.

Testing for DCM:

• Stethoscope testing is a first step to identifying serious cardiac abnormalities, but it cannot identify DCM. Nor can X-ray.
• Gene testing – in 2010 American geneticist Kate Meurs discovered one of the genetic mutations responsible for causing Dilated Cardiomyopathy in Dobermanns and is not consistent with the disease European Dobermanns for some reason. Unfortunately it seemed not to have been the panacea we all hoped for, but good work continues. There have been studies into the Titin gene which are currently progressing very well.
• Troponin testing – Troponin is a protein released by the heart when it is under stress. The test is used in hospitals to distinguish between heart attacks and angina for example.
• Holter Monitor (aka 24 hour tape). A jacket with a device which records the electrical activity of the heart continuously over 24 hours
• Echocardiogram uses sound waves to produce images of the heart beating and pumping blood.

• Update 17.03.2020 from Sue Thorn – Dobermann Breed Health Co-ordinator from Jo Dukes McEwan – UK lead on DCM at Liverpool University:

  Sue writes: I now have the preliminary results of Jo Dukes-McEwan’s research into the use of blood biomarkers for initial DCM testing. She concludes that the biomarkers are an effective first test, provided lower threshholds are used, aboive which echo and Holter are carried out. The summary is below.
  Cardiac biomarkers as primary screening Dobermanns for DCM
  Dr Jo Dukes-McEwan and colleagues have been researching use of blood biomarkers for diagnosis for some years. A project funded by the Dobermann community and the Kennel Club Charitable Trust sought to establish whether the two blood biomarkers – Cardiac Troponin I (cTnI) and N-terminal pro-BNP (NTproBNP) – used together, would be a better predictor of occult DCM (ie before symptoms appear) than either separately, and whether these could be used as a reliable, low-cost first-line test, reserving the more expensive echo and 24-hour Holter tests for follow-up where indicated.
  Dr Dukes-McEwan’s preliminary results conclude that the two biomarkers together are an adequate initial test for DCM, provided cut-offs of 0.06 ng/mL are used for cTnI and 626 pmol/L for NTproBNP. These are lower than the current cut-offs of 0.07 and 900. Results above these cut-offs do not necessarily mean that the dog has DCM, nor that it will develop DCM, as other health issues can cause elevated results, but it does mean additional testing is indicated by echo and Holter.
  The research is based on results of tests on 59 Dobermanns without DCM (as tested by echo and Holter) and 52 already diagnosed with DCM (based on echo, Holter or both). The research showed that, when the two tests are used together, ROC analysis area under the curve was 0.876 (where 1.0 is a perfect test and 0.5 is a random results). This is better than either separately and means that, of an average 100 dogs tested, it will correctly identify DCM status in almost 90%, compared to use of echo and Holter. We have nothing better with which to compare echo and Holter, so we can’t say what percentage those tests identify correctly.
  This summary is based on a short abstract published in the proceedings of the 2020 BSAVA conference. The full paper will be submitted in due course.

To examine the hips for scoring, dogs are sedated and x-rays are taken when the dog is lying on its back. The aim is to see how well the hip joint fits into the socket. The hip scoring panel assess the x-rays and grade the hips on 7 different aspects of fit and function. Each aspect of each hip is assigned a numerical score with 0 being excellent and 53 being the worst. The total score available is 106 The supposed* ‘average’ UK score is a total of 10.

It is uncommon to see severe dysplasia in Dobermanns. HD is primarily hereditary, although environmental factors such as a high protein diet and over exercise in puppies may play a large part in the development of the disease. X-Rays can be carried out usually from one year of age. The mode of inheritance of Hip Dysplasia is unknown, as identifying the gene marker responsible for HD is not possible given the variable scores of each factor. The pelvis and surrounding area is also taken into consideration on the overall score. Parents with excellent scores can produce progeny with very poor scores – ie two GSD brothers we knew of who were raised in the same household, on the same diet with the same environmental factors. Parents were 0:2 and 2:2, grandparents were 1:0, 2:1, 1:0 and 3:2, produced the brothers – one was scored at 4, the other at 86.

Generally the higher the score, the higher probability of clinical signs of the disease in the dog. Scoring is not an exact science. Is 15; 20; 25; 30; 40, 50 a ‘bad’ score? There is no figure at which any particular dog becomes clinically dysplastic. Although hip scoring is such an inexact science and as a clinical test is relatively worthless as a predictive tool, I continue to hip test to enable me to avoid mating two high-scoring dogs.

Why would any breeder use a dog above the ‘UK average?

With an average of 3,000 registrations annually, and around 30 dogs scored annually, 1% is wholly insufficient to gain a true average. The BVA idealistically state: “Breeders wishing to reduce the risk of HD should select their breeding stock (both dogs and bitches) only from animals with hip scores well below the Breed Mean Score. Many clinically sound dogs may have high HD scores and should not therefore be used for breeding”. This utter idealism by the BVA can exclude otherwise magnificent dogs from breeding, and reduces the gene pool of otherwise healthy dogs by removing a dog with one comparatively ‘poor’ score from breeding. Probably only a handful of breeding dogs and bitches have scores ‘well below’ 10.

Aritaur dogs range from a very low 2:2 (4) to one dog with a 32:32 (64) score and our average hip score is a total of 9. Nutrition, early exercise and particularly early castration has a major effect on hips. Whilst it can’t alter the shape of the socket, the degree of laxity could be altered.

PHPV (Persistent Hyperplastic Primary Vitreous) is an eye condition which can but rarely causes loss of vision. As with human infants, puppies are born with a shield of primary vitreous (membrane) covering the immature eye. ‘Persistent’ ie does not disappear by 7 weeks as it should, means it leaves strands which may interfere with vision. Very few dogs are tested in the UK and a grading is not given as it is in some European countries, so we do not know how much of a problem it is in the breed in the UK but it seems of low incidence. Scandinavian countries (notoriously the toughest for grading of all health tests) allow breeding a dog with a grade of up to 2/3 to a Clear partner. Without a grading system in this country, dogs with just the equivalent to Grade 1 with a tiny piece of primary vitreous in the corner of an eye, which will never progress or hinder sight and which will not necessarily be passed on, could be wrongly excluded from the gene pool for no good reason whatsoever. The other breeders in the KC Assured Breeder Scheme and I have made it very clear to the Kennel Club that we will not be adhering to the new rule from the British Veterinary Association to have dogs eye tested annually. PHPV is the only listed condition that Dobermanns can develop, and it is not a progressive disease, so testing annually is in our opinion is meaningless and purely lines the pockets of the opthalmologists. Give us a grading system and we might. Once again, the BVA is offering contradictory and idealistic advice.

CS is a degeneration in the structure of the spinal column in the neck resulting in instability between the vertebrae and placing pressure on the spinal cord. This results in compression or instability on the spinal cord resulting in loss of hind co-ordination and the classic wobbly hind legs.

It may be caused by congenital abnormality, birth defect, trauma and possibly genetics although this has never been proven to any satisfactory conclusion (see below). In mild cases there may be just local tissue swelling resulting in neck pain, stiffness and swelling, but either way (and the term wobblers encompasses all possible causes) it results in lack of co-ordination in the hind legs. Examination by X-Ray can be carried out usually from one year of age. During the 80’s and 90’s, there was a programme at Liverpool University of neck scoring Dobermanns to identify hereditary cause of the disease. Unfortunately, testing was found to be an unreliable method of identifying which dogs would develop the problem, with progeny from normal parents being affected and vice versa. The disease can be instigated by injury. Early exercise and diet may be factors as it is in HD, and although severe malformation in puppies is rare, this could equally be caused by