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Health Issues In The GSD

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Long Term Effects of Malnutrition/Starvation

Sadie is a sweet female, about 8 years old, that had been fending for herself for a long time. Though her coat is nice, when she arrived at rescue, it was matted and dirty. Still, since she is heartworm negative and does not have fleas, we suspect she may have been dumped by her previous owners. When she came to rescue, Sadie was so underweight that she has muscle wasting from her body. This was from a long term starvation, 4 to 6 months at least.

The lovely Miss Sadie has been into rescue now for several weeks and has put on a little weight but a dog in this condition can not eat lots of food to gain too quickly. Many small meals a day are needed to avoid kidney failure. We began by giving her 8 meals a day (about 1/4 cup at a time and have been increasing the amount every few days). Her vet exams have gone well and her hips and spine are good but she has such little muscle that she can only walk or play ball (which she loves) for a few minutes at a time.

Wasting is sometimes referred to as "acute malnutrition" causing muscle and fat tissue to "waste" away. The body will combat malnutrition by breaking down its own fat and eventually its own tissue.
Characteristic symptoms of starvation include:

* shrinkage of vital organs, such as the heart & lungs
* chronic diarrhea
* anemia
* reduction in muscle mass and weakness because of it
* low body temperature
* decreased ability to digest food because of lack of digestive acid production
* irritability
* immune deficiency
* swelling from fluid under the skin

UPDATE:  January 2010 Tampa Bay German Shepherd Rescue got her her through the diarrhea and the swelling from the fluid.  She was digesting her food well,  still being fed multiple times a day. Given the TLC she has missed, Sadie finally knew the love she should have known all her life.  Sadly, though she didn't make it.  We lost her despite all our best efforts.  It nearly breaks our hearts every time we get so emotionally invested and then lose such a wonderful dog, but we know that her last days were good ones and she knew she was loved.

Diagnosis of DM is made by a history of progressive spinal ataxia and weakness that may have a waxing and waning course or be steadily progressive. This is supported by the neurologic findings of a diffuse thoracolumbar spinal cord dysfunction. Clinical pathologic examinations are generally normal except for an elevated cerebral spinal fluid (CSF) protein in the lumbar cistern. Electromyographic (EMG) examination reveals no lower motor unit disease, supporting the localization of the disease process in the white matter pathways of the spinal cord. Spinal cord evoked potentials recorded during the EMG do show changes which help determine the presence of spinal cord disease. Radiographs of the spinal column including myelography are normal (other than old age changes) in uncomplicated DM. Unfortunately, myelography can be associated with worsening of clinical signs and carries some degree of risk for certain patients.

During the past two decades, we, at the University of Florida, have provided important new insights into the pathoetiology of DM. The release of antigens during the disease process could explain the immune deficits seen in DM and suggests that processing these immune-complexes by circulating macrophages leads to the development of the circulating suppressor cells that were previously noted. 

This provides a logical explanation for the presence of immune abnormalities in GSD with DM. Electrophoresis of immune-complexes demonstrates that the proteins present are inflammatory proteins which increase in inflammatory diseases of the dog nervous system. It is hoped that working with the antigens present in the immune-complexes will lead to a major breakthrough in our understanding of DM and that this also could lead to an early serodiagnostic test for the condition. However, the development of a serodiagnostic test will await the availability of antibodies specific to unique markers within the inflammatory proteins of DM dog immune-complexes. However, the development of a serodiagnostic test will await the availability of antibodies specific to unique markers within the inflammatory proteins of DM dog immune-complexes. 

While the cause of the altered immune system is not known, what is increasingly clear is that DM is caused by an autoimmune disease attacking the nervous systems of patients, leading to progressive neural tissue damage. In many respects, DM is similar to what has been discovered about the pathogenesis of Multiple Sclerosis in human beings. In fact, based upon new data concerning the pathology of MS, we can now say with some degree of certainty that DM is MS in dogs. We believe that, due to some triggering factor, immune-complexes circulate. These immune-complexes lead to
endothelial cell damage in the vessels of the CNS. Subsequently, fibrin is deposited in the perivascular spaces. When this degrades (point of action of aminocaproic acid), inflammatory cells are stimulated to migrate into the lesions. The inflammatory cells release prostaglandins and cytokines (point of action of vitamin E and C) which leads to the activation of tissue
enzymes and the formation of oxygen free-radicals (point of action of acetylcysteine) which, in turn, leads to tissue damage. Treatment of DM of GSD, which we recommend, is directed at these pathologic processes. 

The Integrative Medical Approach to Treatment of Degenerative Myelopathy:
The treatment of DM involves four basic approaches: 
1) exercise 
2) dietary supplementation 
3) medication 
4) other supportive measures

"Alvin, we have sent you on a journey to a land free from pain, not because I did not love you, but because I loved you too much to force you to stay."  -Diane Roberts

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