Dilated Cardiomyopathie (DCM)
What is it?
DCM is a disease of the heart muscle that results in weakened contractions and poor pumping ability. As the disease progresses the heart chambers become enlarged, one or more valves may leak, and signs of congestive heart failure develop. The cause of DCM is unclear in most cases, but certain breeds appear to have an inherited predisposition.
Large breeds of dogs are most often affected, although DCM also occurs in some smaller breeds such as cocker spaniels. Occasionally, DCM-like heart muscle dysfunction develops secondary to an identifiable cause such as a toxin or an infection. In contrast to people, heart muscle dysfunction in dogs and cats is almost never the result of chronic coronary artery disease (“heart attacks”).
What are the signs of this disease?
Early in the disease process there may be no clinical sign detectable, or the pet may show reduced exercise tolerance. In some cases, a heart murmur (usually soft), other abnormal heart sounds, and/or irregular heart rhythm is detected by your veterinarian on physical examination. Such findings are more likely as the disease progresses.
As the hearts pumping ability worsens, blood pressure starts to increase in the veins behind one or both sides of the heart. Lung (pulmonary) congestion and fluid accumulation (edema) often develop behind the left ventricle/atrium. Fluid also may accumulate in the abdomen (ascites) or around the lungs (pleural effusion) if the right side of the heart is also diseased. When congestion, edema and/or effusions occur, heart failure is present. Weakness, fainting episodes, and unfortunately, even sudden death can result from heart rhythm disturbances (even without “heart failure” signs).
What are the signs of heart failure?
Dogs with heart failure caused by DCM often show signs of left-sided congestive failure. These include reduced exercise ability and tiring quickly, increased breathing rate or effort for the level of their activity excess panting, and cough (especially with activity). Sometimes the cough seems soft, like the dog is clearing its throat. Poor heart pumping ability and arrhythmias can cause episodes of sudden weakness, fainting, or sudden death as noted above. Some dogs with DCM experience abdominal enlargement or heavy breathing because of fluid accumulation in the abdomen or chest, respectively. Presence of any of these signs should prompt a visit to your veterinarian to determine if heart failure (or another disease) has developed.
More advanced signs of heart failure could include labored breathing, reluctance to lie down, inability to rest comfortably, worsened cough, reduced activity, loss of appetite, and collapse. A veterinarian should be consulted right away if these signs occur. Signs of severe heart failure may seem to develop quickly with DCM, but the development of underlying heart muscle abnormalities and progression to overt heart failure probably takes months to years.
How is this disease diagnosed?
A cardiac exam by a veterinarian can detect abnormal heart sounds (when present) and many signs of heart failure.
Usually chest radiographs (x-rays), an electrocardiogram (ECG), and echocardiogram are performed to confirm a suspected diagnosis and to assess severity. Echocardiography also can be used to screen for early DCM in breeds with a higher incidence of the disease. Resting and 24-hour (Holter) ECGs are sometimes used as screening tests for the frequent arrhythmias that usually accompany DCM in some breeds, especially boxers and Doberman pinchers.
What can be done if my pet has this disease?
Asymptomatic (subclinical) cases of DCM may be treated with enalapril or another ACE inhibitor to slow progression of the changes leading to heart failure. Other medications and strategies are also used as signs of heart failure develop and/or if rhythm abnormalities are present. Therapy is always tailored to the needs of the individual patient. Since this disease is not reversible and heart failure tends to be progressive, the intensity of therapy (for example, the number of medicines and the dosages used) usually must be increase over time.
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 raport (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.
Grade 1: Retrolental fibrovacsular pigmented dots (with a diameter about 0,1 mm) alone on the
posterior capsule of the lens
Grade 2: Dots in combination with a retrolental tissue proliferation (plaque), attached to the posterior
Grade 3: Plaque in combination with persistent parts of the hyaloid (-TVL) vascular system
Grade 5: Plaque, lenticonus posterior, and persistent parts of the hyaloid-TVL system (a
combination of grades 3 and 4)
Grade 6: 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 vision.
In grade 1 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 another 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 color 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 courages to be executed by the breeder. The examination is performed 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 dyslasia (HD)
To understand hip dysplasia we must have a basic understanding of the joint that is being affected. The hip joint forms the attachment of the hind leg to the body and is a ball and socket joint. The ball portion is the head of the femur while the socket (acetabulum) is located on the pelvis. In a normal joint the ball rotates freely within the socket. To facilitate movement the bones are shaped to perfectly match each other; with the socket surrounding the ball. To strengthen the joint, the two bones are held together by a strong ligament. The ligament attaches the femoral head directly to the acetabulum. Also, the joint capsule, which is a very strong band of connective tissue, encircles the two bones adding further stability. The area where the bones actually touch each other is called the articular surface. It is perfectly smooth and cushioned with a layer of spongy cartilage. In addition, the joint contains a highly viscous fluid that lubricates the articular surfaces. In a dog with normal hips, all of these factors work together to cause the joint to function smoothly and with stability.
Hip dysplasia is associated with abnormal joint structure and a laxity of the muscles, connective tissue, and ligaments that would normally support the joint. As joint laxity develops, the articular surfaces of the two bones lose contact with each other. This separation of the two bones within the joint is called a subluxation, and this causes a drastic change in the size and shape of the articular surfaces. Most dysplastic dogs are born with normal hips but due to their genetic make-up (and possibly other factors) the soft tissues that surround the joint develop abnormally causing the subluxation. It is this subluxation and the remodeling of the hip that leads to the symptoms we associate with this disease. Hip dysplasia may or may not be bilateral; affecting both the right and/or left hip.
What are the symptoms of hip dysplasia?
Dogs of all ages are subject to hip dysplasia and the resultant osteoarthritis. In severe cases, puppies as young as five months will begin to show pain and discomfort during and after exercise. The condition will worsen until even normal daily activities are painful. Without intervention, these dogs may eventually be unable to walk. In most cases, however, the symptoms do not begin to show until the middle or later years in the dog’s life.
The symptoms are similar to those seen with other causes of arthritis in the hip. Dogs often walk or run with an altered gait. They may resist movements that require full extension or flexion of the rear legs. Many times, they run with a ‘bunny hopping’ gait. They will show stiffness and pain in the rear legs after exercise or first thing in the morning. They may also have difficulty climbing stairs. In milder cases dogs will warm-up out of the stiffness with movement and exercise. Some dogs will limp and many will become less willing to participate in normal daily activities. Many owners attribute the changes to normal aging but after treatment is initiated, they are surprised to see a more normal and pain-free gait return. As the condition progresses, most dogs will lose muscle tone and may even need assistance in getting up.
Who gets hip dysplasia?
Hip dysplasia can be found in dogs, cats, and humans, but for this article we are concentrating only on dogs. In dogs, it is primarily a disease of large and giant breeds. German Shepherds, Labrador Retrievers, Rottweilers, Great Danes, Golden Retrievers, and Saint Bernards appear to have a higher incidence, however, these are all very popular breeds and may be over represented because of their popularity. On the other hand, sighthounds such as the Greyhound or the Borzoi have a very low incidence of the disease. This disease can occur in medium-sized breeds and rarely in small breeds. It is primarily a disease of purebreds although it can happen in mixed breeds, particularly if it is a cross of two dogs that are prone to developing the disease.
What are the risk factors for the development of hip dysplasia?
Hip dysplasia is caused by a subluxation in the hip joint. This creates abnormal wear and erosion of the joint and as a result arthritis and pain develop. The disease process is fairly straightforward; the controversy starts when we try to determine what predisposes animals to contracting the disease.
Genetics: Researchers agree that hip dysplasia is a genetic disease. If a parent has hip dysplasia, then the animal’s offspring are at greater risk for developing hip dysplasia. If there are no carriers of hip dysplasia in a dog’s lineage, then it is highly unlikely he will not contract the disease. If there are genetic carriers, then he 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 the offspring 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 will most likely show up in their offspring in later generations. This is why it can be challenging to eradicate the disease from a breed or specific breeding line.
von Willebrand disease (vWD)
Von Willebrands Disease is the most common of bleeding disorders in dogs and humans. Symptomsdiagnosis and general information of the condition
Von Willebrand’s isn’t so much a disease as a condition. Of all the inherited bleeding disorders in animals (and humans) it is the most common. The defect isn’t autosomal (sex linked) so both males and females can suffer from the “disease.” It must be remembered that just because a dog doesn’t show symptoms of von Willebrand’s, it doesn’t mean it can’t be a carrier.
Von Willebrand’s was discovered in humans and called a “disease” in the 1920s by a Finnish doctor coincidentally named, von Willebrand. After further research, he was able to figure out the illness was actually linked to a missing factor in the blood’s clotting ability.
Modern research has found von Willebrand’s doesn’t lower the number of platelets (the factor in the blood that causes clotting) but changes the platelet’s actual make up. Researchers have discovered there are twelve “factors” that go into the platelet’s make up and allows them to work properly. They have set up a “Cascading Clotting Tree” to mark and show the different factors. Von Willebrand’s affects Factor 8 on this tree.
There is a large, multimeric glycoprotein that is labeled as vWF. This glycoprotein circulates in the plasma and is required for platelet adhesion. When there is a defect in the vWF gene, there is an insufficient synthesis of the vWF glycoprotein. This insufficiency causes the platelets to fail in their adhesion or “sticking together.” Like water coming through a damn with a hole in it, the platelet “leaks” and bleeding continues.
Von Willebrand’s seldom happens in cats but it is very common in various breeds of dogs. In all, some sixty different purebred breeds have been commonly linked to von Willebrand’s with the Dobermann Pinscher having the highest incidence. Clinical trials conducted on 15,000 Dobermanns showed seventy percent of them were carriers of the disease. Of these 15,000 Dobermanns, the majority of them didn’t show clinical signs. Another study estimated 68%-73% of Dobermanns had the disease
Although Dobermans are the most commonly affected by von Willebrand’s Disease, they usually have the milder forms. It is also one reason Dobermanns have such a lower survival rate of diseases such as Parvovirus, which attacks the gastro-intestinal tract and causes bleeding.
Other breeds that have a high incidence of von Willebrand’s disease are Shetland sheepdogs, Scottish terriers, Airedale terriers, Bassett hounds, Dachshunds, German shepherds, Keeshonds, Corgies, Rottweilers, Poodles, Schnauzers and Golden retrievers.
Often von Willebrand’s will show no clinical signs until the dog begins bleeding for some reason. This reason could be something as simple as a nail trim, spay or neuter or a heat cycle in females or even teething in a puppy. While some dogs never show clinical signs of the disease, others may have nosebleeds or vaginal or penile bleeding. Bleeding from the urinary tract, gums or other mucous membranes and hemorrhaging under the skin are all common symptoms of von Willebrand’s Disease. Females with von Willebrand’s may experience excessive bleeding after whelping (giving birth).
There are three classifications of von Willebrand’s disease:
Type I – low vWF concentration. This is the most common of types and is typical of Dobermanns,
Airedales and at least one-third of Shelties. The clinical symptoms may vary in severity
Type II – Uncommon form of von Willebrand’s that is attributed to German Shorthaired Pointers.
Type III – The most severe of types. It has the highest deficiency of vWF and is a typical defect in
Scotties, Chesapeake Bay retrievers and the remaining two-thirds of affected Shelties.
Studies have shown hyperthyroidism may raise the risk of bleeding complications in animals that have von Willebrand’s Disease.
To diagnose von Willebrand’s Disease a veterinarian will often conduct a CBC (complete blood count), urinalysis, blood clotting time or a “buccal mucosal” screening time. The buccal mucosal bleeding time uses a test strip that is tied around the maxilla (upper jaw) that then causes engorgement in the folded-back area. Normal blood clotting time is somewhere between 1.5 to 2.6 minutes.
It is interesting to note many Dobermans and other high risk breeds may go through routine ear trims, tail docks, early spays or neuters and show no signs of von Willebrand’s then at a much later time in their life show the classic symptoms.
There is no cure for von Willebrand’s but there are some precautions an owner can take to reduce the risks to their dog. Avoid drugs that are known to inhibit platelet functions. Aspirin is a prime example of one of these
drugs. Others include antihistamines, sulfa- or penicillin based antibiotics, Ibuprofen, the tranquilizer phenothiazine, heparin and theophylline.
Veterinarians have found that thyroid supplementation can lower the tendency in some dogs to bleed while raising the level of vWF concentration.
There is also a drug called DDAVP that can also increase the vWF protein concentration although the response to the drug is variable. It has been shown to raise the concentration in dogs that do not have von Willebrand’s disease. The use in these dogs may not be apparent until it is realized it takes a dog to donate blood for a transfusion to another dog. In case of an emergency or severe trauma, this donated blood is often the only thing that can save the dog’s life.
For owners of breeds that are more prone to having von Willebrand’s disease, there is a specialized test that can determine the exact amount of the von Willebrand protein that is present in the blood. If the test comes back positive for the disease, it won’t necessary help the dog on a daily basis but will come in handy to know if the dog ever requires emergency treatment or undergoes any type of surgery.
Von Willebrand’s disease isn’t an automatic death sentence to dogs. Many of the dogs that have the condition will live normal lives with no complications. For those that do show clinical signs, there are always options for the owner to guarantee the best quality of life the pet can have.