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Muscular Dystrophy in Rottweilers

Muscular Dystrophy in Rottweilers

By Lew Olsen • Summer 2000 Newsletter
The hardest issue for any breeder to recognize and confront is a problem in their own bloodlines. It is a tough decision to be open and honest with problems we discover in our own puppies and be willing to share this publically. My hope in sharing this information is that some breeders will recognize this problem as something they have seen before and contact me so more information can be gathered. My other expectation is to encourage breeders not to put these puppies down, but to understand they can live a good life. Please don’t discard them just because they have a different appearance than other Rottweilers or for fear people will discover you may have a health issue in some your puppies.

In the spring of 2000 I was fortunate enough to have one of my girls whelp ten healthy puppies. The births were uneventful and the puppies continued to thrive until four weeks. At that point I noticed one of the males was down on his pasterns. This concerned me as I had seen a similar a puppy four years prior which it turned out to have a heart murmur and a subsequent heart doppler and exam showed he might have Sub Aortic Stenosis. This is a genetic heart problem that can result in death. (I would recommend testing and clearing for this disorder before breeding any Rottweiler).

I took this current puppy right in for a heart exam. The initial results showed a heart that was clear. I was still very concerned. I continued with treatment for him to help with improving ligament strength which included digestive enzymes, probiotic powder and organic apple cider vinegar. Much to my relief, his pasterns begin to strengthen.
When it came time for placement of the puppies, something told me to hold on to this one. He appeared normal and many of the buyers expressed interest in him, but I declined. He played normally with the other puppies and had an outgoing personality. He presented no mobility problems but I remained suspicious.
At twelve weeks I took him and his sister in for a modified live parvo and distemper vaccination, and things changed drastically after that. His sister showed no ill effects, but this puppy began show lethargy. He also begin to show slight fevers, lost his appetite and began to became weak in his rear. He became very cow hocked, went back down in his pasterns and his front feet began to splay. His back became hunched and he most often slept or laid down to rest. This began the first of his many visits to veterinarians.
We first thought he had a vaccination reaction, but his symptoms seemed too severe for that. My local vet made a referral toTexas A&M Vet School in College Station, Texas. Upon their initial investigation they asked me about his diet. When I informed them he ate a raw diet, I could see the disapproval in their faces. I continued to ask for a neurological exam but after the radiographs they proclaimed him to have HOD (hypertrophic osteodystrophy). This is an inflammation in the weight carrying bones caused by unknown reasons. It causes slight boney changes in the joints. One reason can be a calcium/phosphorus imbalance, so they immediately decided it was his diet. This was very frustrating for me, as he was from a litter of ten and all were receiving the same diet. It seemed improbable that only one puppy would show these symptoms.
I had a parathyroid test run on him through my local vet (which shows the calcium/phosphorus levels) which proved my puppy was normal in this area. Another trip to a radiology specialist showed this puppy did not have HOD. Meanwhile, my puppy was continuing to become weaker and more fragile. I called Dr. Jean Dodds of Hemopet in Santa Monica, California who quickly advised using prednisone to try and save relieve his symptoms. She said it could be vaccine related but I needed to continue to pursue whatever health issues that could be contributing to this. (Further research showed that HOD is not caused by diet, but may be triggered by the distemper vaccination or a tumor on the parathyroid gland).
The prednisone made a dramatic improvement. He was eating and back on his feet within hours, and his fevers stopped.
With the help of the radiologist and my local vet, A&M agreed to see him once more. I had written a letter to the nutritionist at A&M and he agreed he had misread the puppies diet and the calcium/phosphorus levels were fine. I was able to demonstrate to him that his computer programs for calculating nutrient levels did not have the capability to include the bones from the meat I fed this puppy. He also agreed that diet did not cause HOD as first assumed and was gracious enough to refund part of my money spent on the first visit at A&M.
I had done much of my own research at this time and was convinced this puppy had a neurological problem as I first suspected. I had been looking at the numerous types of muscular dystrophy. The neurologist at A&M agreed with me and decided to take a muscle biopsy sample to send for diagnosis. She was also helpful in providing me with two articles written specifically on Rottweilers with neuromuscular problems. As I read the articles provided, I found two types that fit the description of my puppy.
Coincidentally, during the wait for this second appointment the owner of the puppy with the suspected SAS called me. She told me her marriage had ended and she could no longer keep him. She now lived in Chicago and agreed to bring him to me (I always take puppies back, regardless of the age with no questions asked). Kenny was now four years old.
As soon as she arrived and Kenny got out of the car, I realized right away that he looked very similar to my puppy, Tim. He presented the same rear end weakness with badly turned in hocks, a hunched back and muscle atrophy in the legs, head, shoulders and pelvis.
We were also amazed as Kenny’s diagnosis of SAS had given him one year to live and he had already beaten those odds by three more years of life. He was happy, healthy and bouncy…. but a very narrow, cow hocked dog who bunny hopped when he ran. He also became tired easily. He could run and jump but could not stand for long periods of time and preferred to sit. These are the same symptoms Tim showed. Also his front feet were flat and splayed.
I called the neurologist who was “excited” and asked me to bring Kenny along to Tim’s appointment so she could examine him and we could perform another doppler on Kenny, and one on Tim as well.One problem that occurred from the surgery and anesthesia is that the trauma set Tim back quite a bit in his progress. Another problem was that his incision took a long time to heal and became infected. I noted in one of the case studies the neurologist gave me is that recovery from the incision can be a problem with puppies with muscular dystrophy.
Kenny’s doppler showed his heart had much damage (especially thickening of the heart wall) but the cardiologist noted damage not really comparable to SAS. Tim’s doppler did show some compromise in the heart, although not as severe as Kenny.
The results were promising, but not entirely what I had hoped for. The neurologist had taken a wrong muscle sample for submission. While this sample showed evidence of suspected distal myopathy, another sample from the correct muscle was needed for a specific diagnosis. I declined due to the repercussions of the first procedure.I opted instead to try the supplements that were found helpful in some of the test subjects. I was told giving my puppy these would make any further tests inconclusive, but I felt his health and well being were more important than a definitive diagnosis.The supplements recommended included 100 mg of l-carnitine per kg of the dog’s weight. The l-carnitine helps prevent fiber buildup in the muscles. Also recommended is COQ10 (I give Tim 60 mg twice a day) and a vitamin B complex. He also gets 10,000 mg of l- glutamine a day as recommended on several websites for humans with muscular dystrophy. This helps prevent much of the muscle atrophy. These are many of the same supplements bodybuilders use to increase muscle mass.
Initially the neurologist was very interested in pursuing the puppies pedigree and information, and this excited me as well. However, once she realized she has taken the wrong muscle biopsy and the test was inconclusive all interest was lost.
I am writing this article in hopes of finding other people with Rottweilers with these symptoms. I really believe we need to get these dogs diagnosed, study the disease, be able to name it and examine the mode of inheritance. I know this takes courage on the part of breeders, but I will also guarantee anonymity for these breeders if they contact me. I feel Muscular Dystrophy is more prevalent in our breed than most will admit and I think we need as much information as possible. Please help me in finding out more about these disorders. The more cases we find, the more interested neurologists will become in pursuing and studying this problem.
In the last fifteen years, I have personally seen six Rottweiler puppies that I know probably presented this disorder. I have spoken to numerous other breeders who upon reflection spoke of puppies they have seen like this as well. I am aware of about fifteen that may have one of the symptoms listed below, which appear to be most probably distal myopathy. There are several interesting points to note here including:
Generally only one or two puppies are affected per litter.
Of the cases I have found, only two were females.
Severity of symptoms can vary greatly and generally start at about four weeks. They generally wane for a short period and then come back at around 12 weeks (This can vary too).
Diagnosis is difficult and most puppies are euthanized (much to my disappointment as I would loved to see continued monitor of them as they aged).
Heart involvement is seen in most of them, if a doppler is used The heart condition can vary from mild to severe. The heart afterall is simply a muscle.
Often the puppy won’t show obvious symptoms until 9 to 14 weeks, often after they have left the breeders home.
These puppies may be prone to immunity problems including vaccination reactions (especially from the MLV distemper shot, kennel cough, poor wound healing, allergies, skin problems and pneumonia.
There are two main types of Muscular Dystrophy that have been found in Rottweilers. These are Canine X-linked MD and Distal Myopathy of Rottweiler Dogs. The information I have found on both these diseases are from articles and research done by Dr. G. Diane Shelton, D.V.M. PhD.It is unclear to date which of these disorders Tim and Kenny present (although distal myopathy seems more likely, Canine X-linked causes early death) and I hope to do more testing in the future. Both are felt to be similar to Duchenne Muscular Dystrophy found in humans.
Canine X-linked MD
This is found in Golden Retrievers, Samoyeds, Bouvier Des Flandres, Irish Terriers, Brittany Spaniels, Miniature Schnauzers, Groenendaleler Shepherds and Rottweilers. Symptoms using develop at 6-9 weeks. These include muscle atrophy, irregularities of the spine (such as a hump on the back), low tolerance to exercise, swallowing and esophageal problems, stiff movement with shuffling, enlargement of the base of the tongue and a weak bark. In humans with Duchenne MD one will often see large calves (not muscle but fiber build-up). This can also be seen in the thigh muscles of affected dogs. This disorder is caused by a lack of the bodies ability to make dystrophin which is found on the inner side of muscle fiber. These fibers then break down.
Normally the body can make these fibers, a dog with this disorder can too during the first few months but then they lose the ability as they mature. X linked recessive disorders are sex linked genes. The female passes an X gene to her offspring (females being XX) while the male has either an X or a Y (males being XY). This disorder is only carried on the X gene. If the mother is a carrier, she can pass the gene to either her sons or daughters. The father can pass either gene, with a Y gene making the egg a male and the X gene producing a female offspring. The gene is only passed on the X gene, so a male cannot produce male carriers. However, all females born to a male carrier will be carriers. If the mother is a carrier, half of her offspring can be unaffected and the other half carriers or affected. In humans a few cases can be genetic mutations, but this is rare. Since this disease affects the muscles, the heart can also be affected. Some may even have respiratory problems and be prone to coughing and pneumonia.
Distal Myopathy of Rottweilers
This disorder affects the distal muscle groups with occasional milder problems in the proximal muscle groups. Symptoms include splayed feet, weak pasterns, poor hock development and strength, low exercise tolerance and atrophy of the muscles. The muscle is replaced with fiber and fatty tissue. Most of these dogs are found to have low levels of l-carnitine in the tissues. Supplements with l-carnitine, B vitamins and COQ10 have found to be helpful, although there is no cure for this disease. The mode of inheritance is unknown at this time. I would suspect it might be similar to Canine X-linked MD although not enough research has been done to date.
Dr. G Diane Shelton D.V.M. PhD from the Department of Pathology at the University of California in San Diego states: “Neuromuscular disorders are some of the most challenging cases confronting the veterinary clinician. While several of these disorders are not treatable, there are those that have specific therapies and can result in a good clinical outcome. A careful clinical evaluation and appropriate diagnostic procedures are essential to obtaining an accurate diagnosis and prognosis. Referral to a board certified specialist with expertise in these types of disorders is usually optimal. There is no such thing as a “table top diagnosis” for any of the neuromuscular diseases. With the exception of a few disorders where a simple blood test can provide the diagnosis such as the acetylcholine receptor antibody test for the diagnosis of acquired myasthenia gravis, the most important diagnostic test for these types of disorders is a properly collected and processed muscle biopsy. Evaluation of muscle biopsies can provide an accurate diagnosis in a large percentage of these cases, allow the muscle pathologist to make an accurate prognosis, and suggest specific therapies” Dr. Shelton does ask dog owners do not contact her laboratory directly, but have a qualified veterinarian who is working with the dog consult and contact her.
Dr. Shelton recommends, as a minimum, following these guidelines for diagnosing neuromuscular problems: Careful physical and neurological examination localizing the clinical problem to the muscle, nerve, or neuromuscular junction Careful history regarding diet, previous drug therapy, travel, and known similar problems in other related animals CBC and serum chemistry panel including creatine kinase (CK) and electrolytes Evaluation of thyroid status (remember that neuromuscular manifestations of hypothyroidism may be the first clinical sign of hypothyroidism!) Acetylcholine receptor antibody titer (acquired myasthenia gravis is a great mimic and can have many clinical presentations) Plasma lactate concentration (an increasing number neuromuscular diseases are being recognized associated with lactic acidemia)
If you suspect you have seen any of these disorders in Rottweilers, please contact me at lewolsen@earthlink.net
Any pictures, diagnosis and lab work information would also be helpful.
Thank you,
Lew Olson
References and further information on these disorders
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