From Breed Predisposition to Disease and Congenital Conditions, from veterinary sources, below are just a few of the food / digestive related known documented problems prevalent [ not fabled ], in the breed :
German Shepherd Dog
* Exocrine pancreatic insufficiency
* Food hypersensitivity
* Gastroenteritis
* Inflammatory bowel disease
And further info [ which is why I asked about the food the young `un is on ] :
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What is exocrine pancreatic insufficiency?
The pancreas has 2 functional parts. The endocrine part secretes insulin and glucagon, which are essential for the metabolism of carbohydrates. The exocrine part consists of units called acini that produce and secrete enzymes essential for the digestion of protein, into the small intestine.
With exocrine pancreatic insufficiency (EPI), there is gradual wasting away (atrophy) of the acini. Clinical signs do not develop until most of the acini are gone. As dogs lose the ability to digest protein, they progressively lose weight despite a voracious appetite.
How is exocrine pancreatic insufficiency inherited?
This is thought to be an autosomal recessive trait in the German shepherd.
What breeds are affected by exocrine pancreatic insufficiency?
There is a genetic predisposition to this disorder in the German shepherd. It also occurs sporadically in dogs of other breeds.
For many breeds and many disorders, the studies to determine the mode of inheritance or the frequency in the breed have not been carried out, or are inconclusive. We have listed breeds for which there is a consensus among those investigating in this field and among veterinary practitioners, that the condition is significant in this breed.
What does exocrine pancreatic insufficiency mean to your dog & you?
Affected dogs lose weight despite voracious appetites, and usually pass large amounts of semi-formed feces. They often eat their own stools, or other inappropriate substances.
Some dogs with this condition do not show these typical signs, and may experience intermittent watery diarrhea or vomiting.
How is exocrine pancreatic insufficiency diagnosed?
The clinical signs of weight loss and increased appetite may occur with malabsorption of nutrients due to a variety of causes. Routine diagnostic tests will eliminate some of these as possibilities. Once EPI is suspected, there are specific laboratory tests that will diagnose this disorder.
For the veterinarian: Assay of serum trypsin-like immunoreactivity (TLI), bentiromide absorption test, and quantitative assay of fecal proteolytic activity (azocasein substrate) are sensitive tests for EPI in the dog. TLI is also a specific test, and requires only 1 sample for diagnosis. (Check with your diagnostic laboratory).
How is exocrine pancreatic insufficiency treated?
Although this disorder can not be cured, management is generally fairly straightforward. Powdered pancreatic enzyme extract is mixed in with each meal. Within a few days, your dog's appetite and stools should become more normal, and s/he will begin to gain weight. Your veterinarian will work with you to determine the best regime (what dose of extract, 1 or 2 feedings per day) to keep your dog free of clinical signs. Enzyme supplementation of your dog's food will be necessary for life.
Some dogs fail to gain weight despite treatment, and this may be due to chronic bacterial overgrowth. A course of antibiotic therapy may be useful in these dogs.
Breeding advice
Affected dogs, and in German shepherds, their parents (considered carriers) and siblings (suspect carriers) should not be used for breeding.
FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.
Copyright � 1998 Canine Inherited Disorders Database. All rights reserved.
Revised: April 27, 2001.
This database is a joint initiative of the Sir James Dunn Animal Welfare Centre at the Atlantic Veterinary College, University of Prince Edward Island, and the Canadian Veterinary Medical Association.
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This gives a good idea of prevalence in Alsatians - please note the red highlighted sentences in the piece below :
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THE PATHOGENESIS OF HYPERSENSITIVITY
Although the gastrointestinal tract has been shown capable of supporting all recognised types of hypersensitivity, it seems likely that IgE is predominantly involved, although some believe that high levels of IgG antibody may be pathogenic. Where local hypersensitivity results, GI disease follows. Systemic hypersensitivity results in the involvement of other systems, and especially the skin.
INCIDENCE
The incidence of food hypersensitivity as a cause of allergic dermatitis is quite controversial, and in many cases food allergy may co-exist with atopy, and a partial improvement only results from feeding a hypoallergenic diet. In general, most clinicians agree that food allergy is much less frequent than is atopy-probably occurring with around 10% of the frequency of the latter.
Food allergy can start at any age, with approximately one third of cases commencing clinical signs prior to one year of age. Thus commencement of clinical signs at a very young age, or after 7-8 years of age will raise the index of suspicion for food allergy as compared with atopy.
Clinical signs
Dermatological signs
Pruritus is present in almost all cases, with a small proportion presenting as severe seborrhoea. Many feel that a primary eruption is more likely to be seen than in atopy. It is a common cause of recurrent pyoderma, and especially folliculitis which relapses very soon after discontinuing the antibiotic therapy.
It has also been shown to be a predisposing cause for German shepherd dog pyoderma (Rosser, 1997).
Distribution of dermatological signs
The distribution of signs in cases of food allergy is highly variable, and is generally not characteristic. They are unlikely to mimic flea allergy, but sometimes they may mimic atopy.
Gastrointestinal signs
These range from the trivial to the severe, and may co-exist with the dermatological signs. Although most authors state that cases involving both systems are in the minority (at most 10-15%), others state that very minor signs, such as increased frequency of defecation-sometimes with soft stools, excessive borborygmi and wind, frequently accompany cases of dermatological disease resulting from food allergy.
In a recent study, every one of 20 cases diagnosed as suffering from adverse food reactions, and presented primarily for dermatological signs, showed some manifestation of gastrointestinal disease (Paterson, 1995)
Adverse reactions to foods resulting in gastrointestinal disease are likely to be far more common that reported in the literature, in that in many cases of diarrhoea and/or vomiting, the owner makes an association with the feeding of different foods, without ever consulting the veterinarian. Chronic gastrointestinal diseases for which food hypersensitivity should be on the top of the list of differentials are canine lymphocytic plasmacytic enteritis, canine eosinophilic gastroenteritis and canine colitis. In all of these, an inflammatory infiltrate with cells known to be involved in immunological responses is seen, and the triggering factor could well be dietary antigen.
Clinical signs
Clinical signs suggestive of food allergy include:
1. Perennial pruritic skin disease in which atopic dermatitis from house dust mite allergy has been ruled out.
2. Intermittent skin disease in animals fed a varied diet.
3. Pruritic disease starting below one year of age, and particularly less than 6 months of age.
4. Distribution of clinical signs that are inconsistent with flea allergy and atopic dermatitis.
5. Co-existence with gastrointestinal signs, which may range from the subtle to the severe.
6. Cases of recurrent pyoderma which relapse quickly after the cessation of antibiotic therapy.
7. Cases in which recurrent otitis externa is a major feature, and where no other cause for the latter can be identified.
Richard EW Halliwell, MA, VetMB, PhD, MRCVS, DECVD
Professor, University of Edinburgh, Royal (Dick) School of Veterinary Studies, Summerhall
Edinburgh, UK
Professor Halliwell received his veterinary training at Cambridge. He then spent two years in surgery at the University of Bristol, followed by 5 years in small animal practice in London. He then returned to Cambridge for PhD studies, before moving to the University of Pennsylvania as Assistant Professor of Dermatology. He then moved to the University of Florida as Chair of the Department of Medical Sciences in the new College of Veterinary Medicine. In 1987 he returned to the UK as William Dick Professor of Veterinary Clinical Studies at the University of Edinburgh.
He has served as President of the both the American and European Colleges of Veterinary Dermatology, and of the American Association of Veterinary Immunology. He recently completed a 4 year term as President of the European Association of Establishments for Veterinary Education.
He is author or co-author of some 100 papers in the area of dermatology and clinical immunology.
References
1. Carlotti, D-N, Vet. Dermatol. 1:55, 1990
2. Jeffers, J et al. J. Am. Vet. Med. Assoc. 198:677, 1991
3. Kunkle G et al. J. Am. Vet. Med. Assoc. 200:245, 1992
4. Patterson, S, J small Anim. Pract. 36:529, 1995
5. Rosser, EJ, J. Am. Vet. Med. Assoc. 203:259, 1993
6. Rosser, EJ, J. Am. Anim. Hosp Assoc 33:355, 1997
7. White, S. J. Am. Vet. Med. Assoc. 188:695, 1986
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I have known many Alsatians with food allergies, sadly there is nothing fabled about it. I would rather try to give answers as to what might be worth exploring than ignore known breed specific problems which MAY be a factor.
My early background, and my familys` before I was born over 40 years ago, is in this breed. Please do not take offence, I just want to try to help.