Causes. The relative frequency of diabetes in the dog is probably dependent on his life in human dwellings and on gourmandizing on dishes prepared for man. Friedberger and Fröhner have produced the disease artificially by feeding a great quantity of sugar and W. Williams has met the disease in dogs fed exclusively and generously on liver. Thiernesse records one case complicated by atrophy and steatosis of the pituitary body, but in all other instances the appreciable lesions were confined to the liver. In one case, reported by St. Cyr, the liver was hypertrophied, yellow, mottled, marked by irregular elevations of congested and hypertrophied hepatic tissue, and showing extensive degeneration—mucous, caseous and fatty. Thiernesse found the liver of a yellowish white color, and the seat of fatty degeneration implicating the hepatic cells. Franzenberg in one case found fatty degeneration of the liver, and Fröhner and Schindelki, in four cases, met with extensive hepatic disease. The macroscopic lesions of the disease in dogs as in horses appear to be mainly hepatic.
On the other hand the complete removal of the pancreas in the dog by Mering, Minkowski, Thiroloix, Lancereaux and others was invariably followed by mellituria, so that even in the absence of clinical examples, we must recognize pancreatic lesions and functional disorders as possible primary causative factors in glycosuria. In the light of experimental medicine we must similarly recognize brain and nervous lesions and reflex actions as possible causes, even if as yet unsupported by clinical facts observed in the dog.
Symptoms. The disease usually appears in an old, fat, pampered dog, affected with dyspnœa or asthma, with dysuria and lameness. The urine is high colored, viscid, and of a high density (1055 to 1060, the normal canine urine being about 1020), and charged with glucose. The subject may have an enormous appetite but fails to gain in weight, and after a time loses flesh and becomes badly emaciated. The pulse is small and frequent, and the temperature which at the outset may reach 102°, falls to the normal as the end approaches. Watering eyes, corneal ulcers, and cataracts as well as hemiplegia and diabetic coma may precede death. The amount of sugar has been found to vary in different cases from 3.2 to 12 per cent. of the urine.
Course. Duration. The dog may live from four to eight months and, as in the horse, sugar may finally entirely disappear from the urine, in connection with the progressive degeneration of the liver. If the patient is unable to take exercise, the case reaches a more speedily fatal issue.
Diagnosis is deduced from the bulimia, pampered condition, breathlessness, thirst, and diuresis, the subsequent loss of condition, ocular troubles, and dropsy or coma, the whole being confirmed by the dense, high colored, viscous, saccharine urine.
Lesions. As already noticed the most constant lesion is hypertrophy of the liver, which is swollen unevenly, has thickened borders, is yellow or red, very friable and often fatty, or caseated. The capsule of Glisson is thickened and fibrous. Hypertrophy and fatty degeneration of the thyroid have been found in different cases and in one instance insufficiency of the mitral valve with systemic venous congestion. Ocular troubles are constant.
Treatment. Put the patient on an exclusive diet of skim or butter milk or if this is impossible it may be conjoined with lean meat—raw or cooked—keep warm and dry, but give plenty of open air and sunshine. Avoid fatigue and over exertion. Restricted diet is of great importance. During the siege of Paris the short rations led to the disappearance of glycosuria from many human patients.
Among medicinal agents, cholagogues come first, sulphate of soda with chloride of sodium, bicarbonate of soda, salicylate of soda, salol, nitro-muriatic acid, may be named. For the febrile condition, antipyrine, acetanilid, or phenacetin may be employed, and iodoform, ergot or codeine may be tried when other measures fail. Bitter tonics and mineral acids may be beneficial, and lastly blisters to the region of the liver may prove of service.
OBESITY AND EMACIATION.
Sugar essential to growth. Ratio of liver to active increase in weight. Obesity and fatty degeneration. Small inactive liver and stunted growth, or loss of weight. Biliary fistula, death in 12 months. Influence of pancreas. Nitrogenous food for obesity, outdoor life, exercise, cholagogues, salines. Saccharine and starchy food for emaciation, hepatic, and pancreatic stimulants. Mild laxatives and cholagogues, pure air, green, succulent food, pure water, bitters, tonics, moderate exercise.