Von Willebrand's disease (vWD) is a common, usually mild, inherited bleeding disorder in people and in dogs. It is caused by a lack of von Willebrand factor (vWF), which plays an essential role in the blood clotting process.
Normally the body responds to an injury causing bleeding through a complex defence system. This consists of local changes in the damaged blood vessels, activation of blood cells called platelets, and the coagulation process. A reduction in von Willebrand factor leads to abnormal platelet function and prolonged bleeding times. Affected dogs are prone to bleeding episodes such as nose bleeds, and generally experience increased bleeding with trauma or a surgical procedure.
Three forms of the disease are distinguished based on vWF concentration and function. Dogs with Type I vWD (by far the most common) have mild to moderate bleeding abnormalities, depending on the level of vWF. The much rarer types II and III vWD cause severe bleeding disorders.
The chart below (provided by VetGen) outlines the implications of various breeding pair combinations. Remember, it is always best to breed "Clear to Clear". If followed by all breeders, these strategies will ensure a significant reduction in the frequency of the targeted disease gene in future generations of dogs. However, to maintain a large enough pool of good breeding stock, it may be necessary for some breeders to breed "Clear" to "Carriers" (see below).
Breeding Pair Combinations CLEAR MALE CARRIER MALE AFFECTED MALE
CLEAR FEMALE 100% Clear 50/50 Carrier/Clear 100% Carrier
CARRIER FEMALE 50/50 Carrier/Clear 25/50/25 Clr./Carr./Affctd. 50/50 Carrier/Affected
AFFECTED FEMALE 100% Carrier 50/50 Carrier/Affected 100% Affected
Ideal Breeding Pair. Puppies will not have the disease gene (neither as Carrier nor as Affected).
Breeding Is Safe. No Affected puppies will be produced. However, some or all puppies will be Carriers. Accordingly, it is recommended that Carrier dogs which are desirable for breeding be bred with Clear dogs in the future, which will produce 50% carrier and 50% clear animals, to further reduce the disease gene frequency. These offspring should be tested by VetGen's test for this defective gene, and if possible, only the clear animals in this generation should be used.
High Risk Breeding. Some puppies are likely to be Carriers and some puppies are likely to be Affected. Even though it is possible that there will be some clear puppies when breeding "Carrier to Carrier", in general, neither this type of breeding pair nor "Carrier to Affected" are recommended for breeding.
So far we have been unable to isolate the DNA effecting the PHPV condition, and so in the UK at this time dogs are assessed to be either affected or clear in regards to PHPV.
PHTVL / PHPV Persistent hyperplastic tunica vasculosa lentis (PHTVL) and persistent hyperplastic primary vitreous (PHPV) refer to the persistence of the embryonic vascular system of the lens.PHTVL /PHPV is a congenital eye anomaly which has been described in many animals as well as in man. Until the late 1970's PHTVL / PHPV was only sporadically described in a litterature in animals including dogs. The first documented case in dog was in a Greyhound (Grimes and Mullaney). After that there were also some descriptions of individual cases of this anomaly in the litterature (Keller, Blanchard and Krehbiel, 1972, Gelatt, 1973, Barnett and Grimes, 1973, Rebhun, 1976, Rubin, 1974, ).
In 1978 a preliminary report (Stades, v.d.Linde-Sipman, Gutteling) and 1980 a more detailed report (Stades) was published in The Netherlands describing the occurence of PHTVL / PHPV in the Dutch Dobermann population. Later this anomaly was reported to exist in the standard Schnauzer (Slatter, 1981), in Staffordshire Bull Terrier (Curtis, Barnett and Leon 1984, Leon, Curtis and Barnett 1986), in Bouviers des Flanders (v. Rensburg, Patrick, v.d.Lugt and Smit, 1992). For to help to better understand and discribe the diversity of the clinical signs of PHTVL / PHPV the Dutch reporters devided the signs into six grades according the severity of the findings. (Boeve, Stades, v.d. Linde-Sipman, Vrensen; Prog Vet & Comp Ophtalmol. Vol 2, No 4) (Figure 1.)
Grade1: Retrolental fibrovacsular pigmented dots (with a diameter about 0,1 mm) alone on the posterior capsule of the lens.
Grade2: Dots in combination with a retrolental tissue proliferation (plaque), attached to the posterior lens capsule.
Grade3: Plaque in combination with persistent parts of the hyaloid (-TVL) vascular system
Grade5: Plaque, lenticonus posterior, and persistent parts of the hyaloid-TVL system (a combination of grades 3 and 4)
Grade6: Abnormal lens shape due to the colobomata or mikrophakia, possibly in combination with the elongated ciliary processes and intra- or retrolental free blood, all in addition to severe (grades 2-5) anomalies.
Grade1 with retrolental dots alone do not develop into a cataract and do not interfere with vision. All other grades progressively worsen and cataract develops. Thus there is a chance of severe impairment or even total loss of a vison.
In grade1 cases the anomaly can be uni- or bilateral. In the more advanced cases it is mostly bilateral, although the severity of the problem can vary in the both eyes. This anomaly is due to an embryological defect in the prenatal ocular development. Normally an arteria (a. hyaloidea) grows from the retinal area through the primary vitreus to the posterior lens capsule. A.hyaloidea forms an vascular net behind the lens and around it (tunica vasculosa lentis). All this is needed to feed the lens and nearby structures. By day 45 of gestation the development of the lens is nearly finished and the network beginns to atrophy. In defected dog there is a metabolic defect and the regression is impaired. Pigment dots against the posterior lens capsule are remnants of the vascular structure failed to atrophy (grade1). In more severe cases there are more advanced defects seen already at the gestation day 35 onward. The problem seems to be originate from the persistence of the vascular structure, thus the name PHTVL is used primarly as a name of this defect. This makes this anomaly different from the human disease where PHPV is described as a non-hereditary mainly unilateral eye defect.
The authors described the heredity to be possibly autosomal incomplete dominant, with variation in the expression ( Stades, v.d. Linde-Sipman, Boeve ). The authors also claim that "a more complex heredity can not be excluded". In onother article the same author suggests a possible interaction of two or three genes.(Stades 1980) There was found no difference in the incidence of the affected dogs between the sexes or among coat colour combinations.
The lens and nearby structures can be examined for PHTVL as early as 7-8 weeks of age. The examination should be done by a veterinarian specialized in eye diseases and with proper slit-lamp biomicroscope equipment. This procedure is strongly courraged to be executed by the breeder. The examination is peformed after inducing total enlargement of the pupils and needs no sedation. It is a common practice to re-exam the dogs before their use in breeding. It is not very easy to discover the grade1 anomaly in a very small and lively puppy at the age of 7 weeks. There appears to be some differences in the results made in a puppyhood compared to the adult result. The anomalies grading higher than 1 are more easy to be recognized even in an early age.
Hip Dysplasia is a developmental disorder of the canine hip joint which is strongly influenced by inherited and environmental factors. It can cause SPONTANEOUS hind limb lameness in a proportion of affected dogs. The condition is often bilateral although lameness may only be seen in one leg. Giant, large and medium sized breeds are most commonly affected although the problem can be recognised in small breeds.
The normal canine hip joint is a tight articulation between the head of the thigh bone (femur) and the deep socket in the pelvis (acetabulum). The femur head should sit within the acetabulum so that more than 50% of its surface is snugly contained. HIP DYSPLASIA describes malformed joints which are loose fitting (lax). This laxity results in an unstable gait, and the femur head rubs unevenly against the rim of the pelvic socket. The joint cartilage is then subject to excessive "wear and tear" and the joint capsule lining becomes inflamed and painful. These processes result in deformity of the bones and arthritis develops.
The current BVA/KC scoring scheme for hip dysplasia (HD) has been in operation since 1984 and since then over 100,000 X-rays have been assessed. Dysplasia means abnormal development, and the degree of hip dysplasia present is indicated by a score assigned to each hip. The hip score is the sum of the points awarded for each of nine aspects of the X-rays of both hip joints. The minimum hip score is 0 and the maximum is 106 (53 for each hip). The lower the score the less the degree of hip dysplasia present. An average (or mean) score is calculated for all breeds scored under the scheme and advice for breeders is to use only breeding stock with scores well below the breed mean score.
The minimum age for hip scoring is one year, and each dog is only ever scored once under the scheme.
The British Veterinary Association uses the following criteria to determine hip score:
Cranial Acetabular Edge
Dorsal Acetabular Edge
Cranial Effective Acetabular Rim
Caudal Acetabular Edge
Femoral Head/Neck Exostosis
Femoral Head Recontouring
The lower the score the less the degree of dysplasia present. The minimum (best) score for each hip is zero and the maximum (worst) is 53, giving a range for the total of 0 to 106.
The following table compares the scores recognised by Orthopaedic Foundation for Animals (OFI), Fédération Cynologique Internationale (FCI), the British Veterinary Association (BVA) and Verein für Deutsche Schäferhunde (SV).
The average score for a Dobermann in the UK is 10 (the sum of both hips)
Dilated Cardiomyopathy (DCM)
Dilated cardiomyopathy is an acquired disease that is characterized by a markedly enlarged and weakened heart muscle. In the Dobermann it affects mainly the left ventricle and left atrium. It results in electrical abnormalities (irregular or abnormal or premature beats). These electrical abnormalities may result in sudden death (described below) as the very first clue of a problem in your dog. Most dogs experience symptoms of pulmonary edema with respiratory distress. DCM is observed in dogs, cats and humans, as well as a number of other species. Dilated cardiomyopathy is always rapidly fatal in the Dobermann.
Most cases of DCM are called idiopathic. This means we do not know the cause of the DCM. Some cases of DCM are due to heart rate abnormalities such as when the heart rate is too high. Other cases are due to a nutritional disorder such as a deficiency of taurine. This does not appear to be the case in the Dobermann. In people, viruses are suspected to cause some cases of DCM. We looked for evidence of parvo virus in Dobermann with DCM and could not find evidence of this virus. In people, an immune mediated disorder (somewhat like rheumatoid arthritis) has been speculated to cause DCM. We looked for evidence of an immune disorder in Dobermann with DCM and could not find evidence of this process at work. In people, about 30% of cases of DCM are familial. Sounds somewhat similar for the Dobermann.
Dobermann may manifest one of two common symptoms related to DCM. Respiratory distress, usually noted as a cough, wheeze, or labored breathing, is the most common symptom of DCM. The next common symptom is called sudden death. In sudden death owners usually observe that their dog was running in the yard then fell over and died. They are dead within a couple minutes. One third of all Dobermann destined to develop/acquire DCM will experience sudden death as the first symptom of their disease. A few dogs are noted to demonstrate a loss of stamina (also called exercise intolerance) as the main sign of DCM.
Occult DCM refers to dogs that have some abnormality with their heart but demonstrate no symptoms for their owners. Thus the owners are unaware that within the chest a problem is stirring. Only when the cardiac disorder becomes more severe do dogs manifest symptoms of heart failure. The current criteria we have observed and are using to indicate that a dog is in the occult stage of DCM is evidence of heart enlargement on cardiac ultrasound (echocardiography) or the presence of irregularities in the heart rhythm (finding PVCs on the ECG). All dogs that are destined to develop DCM and congestive heart failure manifest a time chart (or time line) that goes through three stages. The first stage is characterized by the absence of symptoms of heart disease and a normal heart on all clinical tests (including echocardiography, ECG, Holter, and other tests). The second stage, we are calling occult DCM, is characterized by the absence of symptoms of heart disease but evidence of DCM based on clinical tests (especially echocardiography, ECG, or Holter). The third stage, we are calling overt DCM, is characterized by symptoms of heart failure and evidence of DCM based on clinical tests.
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