Morphologic and immunocytochemical study of young dogs with diabetes mellitus associated with pancreatic islet hypoplasia

In 11 dogs (7 males, 4 females; 10 purebred, 1 mixed breed), diagnosed as having diabetes mellitus before the age of 6 months, the pancreas was evaluated histologically; in 6, the pancreas also was examined by use of electron microscopy and/or immunocytochemical methods. Each dog was placed in 1 of 3 groups (A through C) on the basis of pancreatic histopathologic findings: Group A (n = 3)--no recognizable islets, but the pancreas in 2 dogs contained scattered endocrine cells detectable by use of immunoperoxidase staining or electron microscopy; Group B (n = 4)--no recognizable islets, but the pancreas had severe vacuolation of ducts and acini, as well as acinar atrophy; Group C (n = 4)--scant shrunken islets; 1 pancreas had reduced numbers of recognizable islets, hydropic beta-cell vacuolation attributable to glycogen deposition, and islet and nonislet endocrine cells in expected proportions. Insulitis was not observed in any pancreas, although scattered lymphocytes were seen in the pancreatic interstitial fibrous tissue of 3 dogs. Histologic pancreatic lesions in these young dogs were distinct from those of type-I (insulin-dependent) diabetes mellitus in human beings, as well as from those of diabetes mellitus in aged dogs, but were similar to those described in other young diabetic dogs. This uncommon syndrome is distinct from commonly recognized canine diabetes mellitus, on the basis of age of onset, predisposition for purebred dogs, lack of predisposing endocrinopathies or obesity, and pancreatic histologic features. The cause(s) is unknown, but is related to pancreatic endocrine hypoplasia and not to insulitis or to exocrine pancreatic inflammation. The term pancreatic islet hypoplasia is chosen as best describing this disorder.     

Dermatologic disorders in dogs with diabetes mellitus: 45 cases (1986-2000)

OBJECTIVE: To characterize skin lesions and causative infections in diabetic dogs and evaluate other potential causes of dermatologic disorders, including concurrent endocrinopathies, allergic skin disease, and long-term corticosteroid administration. DESIGN: Retrospective study. ANIMALS: 45 dogs with diabetes mellitus (DM) that were examined by dermatologists. PROCEDURE: Medical records were reviewed for signalment; allergic conditions prior to development of DM; prior corticosteroid administration; and results of dermatologic examinations, ear and skin cytologic examinations, skin scrapings for parasites, bacteriologic and fungal culturing of ear and skin specimens, histologic examinations, and endocrine testing. RESULTS: Bacterial skin infection was the most common dermatologic disorder (n = 38 [84%]), followed by otitis (26 [58%]) and Malassezia-induced dermatitis (19 [42%]). Twenty-two (49%) dogs had pruritic skin disease consistent with allergic dermatitis, which preceded diagnosis of DM. Prior corticosteroid administration was reported in 21 (47%) dogs. Concurrent hyperadrenocorticism was diagnosed in 13 (29%) dogs, and concurrent hypothyroidism was diagnosed in 5 (11%) dogs. Iatrogenic hyperadrenocorticism was diagnosed in 1 additional dog. Only 10 (22%) dogs did not have a documented concurrent endocrinopathy or allergic disease that could have caused the dermatitis. CONCLUSIONS AND CLINICAL RELEVANCE: Bacterial and yeast-induced dermatitis and otitis develop in dogs with DM. Many diabetic dogs with dermatologic problems have a preexisting allergic condition, history of prior corticosteroid administration, or concurrent endocrinopathy that may be a more likely cause of dermatologic problems than DM alone.     

Autoantibodies to pancreatic islet cells in canine diabetes mellitus

Indirect immunofluorescence on normal canine pancreatic tissue fixed in Bouin's solution was used to detect islet cell antibodies in dogs with diabetes mellitus, other endocrine diseases, and pancreatitis. 18 of 25 dogs with diabetes mellitus alone, 2 of 8 dogs with diabetes mellitus and concurrent pancreatitis, and 2 of 2 dogs with diabetes mellitus and concurrent pancreatic exocrine insufficiency were positive for autoantibody. 2 of 12 dogs with hypoadrenocorticism, 3 of 6 dogs with hyperadrenocorticism, 6 of 28 dogs with hypothyroidism and one of 19 dogs with pancreatitis alone were also antibody positive. None of 20 healthy dogs or 20 dogs with disorders other than those of the pancreas or endocrine organs were antibody positive. Islet cell antibodies were demonstrated in dogs with diabetes mellitus and other endocrine disorders. The possibility of autoimmune involvement in the development of diabetes mellitus in the dog should be considered.     

Genetics of canine diabetes mellitus: Are the diabetes susceptibility genes identified in humans involved in breed susceptibility to diabetes mellitus in dogs?

Diabetes mellitus is a common endocrinopathy in companion animals, characterised by hyperglycaemia, glycosuria and weight loss, resulting from an absolute or relative deficiency in the pancreatic hormone insulin. There are breed differences in susceptibility to diabetes mellitus in dogs, with the Samoyed breed being overrepresented, while Boxers are relatively absent in the UK population of diabetic dogs, suggesting that genetic factors play an important role in determining susceptibility to the disease. A number of genes, linked with susceptibility to diabetes mellitus in humans, are associated with an increased risk of diabetes mellitus in dogs, some of which appear to be relatively breed-specific. Diabetes mellitus in dogs has been associated with major histocompatibility complex (MHC) class II genes (dog leucocyte antigen; DLA), with similar haplotypes and genotypes being identified in the most susceptible breeds. A region containing a variable number of tandem repeats (VNTR) and several polymorphisms have been identified in the canine insulin gene, with some alleles associated with susceptibility or resistance to diabetes mellitus in a breed-specific manner. Polymorphisms in the canine CTLA4 promoter and in other immune response genes are associated with susceptibility to diabetes mellitus in a number of pedigree breeds. Genome wide association studies are currently underway that should shed further light on the genetic factors responsible for the breed profile seen in the diabetic dog population.     

Multiple endocrine neoplasia type-I-like syndrome in two cats

Multiple endocrine neoplasia (MEN) embodies a group of diseases in human patients and domestic animals that are characterized by hyperplasia or neoplasia, or both, of two or more endocrine tissues. The MEN-1 syndrome is associated with menin gene mutations that induce various combinations of parathyroid, pituitary, and pancreatic endocrine tumors in humans. Two male, Domestic Shorthair cats developed symmetric alopecia, insulin-resistant diabetes mellitus, and pituitary-dependent hyperadrenocorticism at 12 and 13 years of age. Examination of skin biopsy specimens revealed atrophic dermatosis associated with hyperadrenocorticism. In one cat, cutaneous lesions consistent with paraneoplastic alopecia associated with pancreatic adenocarcinoma also were evident. Multiple invasive pancreatic beta cell carcinomas, pituitary corticotroph adenomas, and thyroid C-cell and parathyroid chief cell hyperplasia were diagnosed on the basis of results of gross, histologic, and immunohistochemical findings in both cats. Pancreatic exocrine adenocarcinoma was diagnosed in both cats. One cat also had hepatocellular carcinoma. Exons 1-8 of the feline menin gene were sequenced and were found to bear 93% homology with the human gene sequence, and the corresponding amino acid sequences shared 98% homology. Purification of total RNA and amplification of cDNA from lesional tissues to document mutations in the feline menin gene sequence were unsuccessful. The combination of lesions observed was consistent with the diagnosis of MEN-1-like syndrome in both cats.     

Endogenous serum insulin concentration in dogs with diabetic ketoacidosis

Objective: To determine endogenous serum insulin concentration in dogs with diabetic ketoacidosis (DKA), and to compare it to endogenous serum insulin concentration in diabetic dogs with ketonuria but no acidosis (KDM), diabetic dogs with uncomplicated diabetes mellitus (DM) that did not have ketonuria or acidosis, and dogs with non‐pancreatic disease (NP). Design: Prospective study. Setting: Veterinary Hospital of the University of Pennsylvania. Animals: Forty‐four client‐owned dogs; 20 dogs with newly diagnosed diabetes mellitus (7 dogs with DKA, 6 dogs with KDM, and 7 dogs with DM) and 24 dogs with non‐pancreatic disease. Interventions: Blood and urine samples were obtained at the time of admission to the hospital. Measurements and main results: Signalment, clinical signs, physical examination findings, and concurrent disease were recorded for all dogs. Blood glucose concentration, venous blood pH, venous blood HCO3^? concentration, urinalysis, and endogenous serum insulin concentration were determined in all dogs. Dogs with DKA have significantly decreased endogenous serum insulin concentrations compared to dogs with DM (P = 0.03) and dogs with non‐pancreatic disease (P = 0.0002), but not compared to dogs with KDM (P = 0.2). Five of 7 dogs with DKA had detectable endogenous serum insulin concentrations, and 2 of these dogs had endogenous serum insulin concentration within the normal range. Conclusions: Diabetic dogs with ketoacidosis have significantly decreased endogenous serum insulin concentration compared to dogs with uncomplicated diabetes mellitus. However, most dogs with DKA have detectable endogenous serum insulin concentrations, and some dogs with DKA have endogenous serum insulin concentrations within the normal range.     

Subepidermal bullous dermatosis due to topical corticosteroid therapy in dogs

Six adult dogs were presented with an unusual bullous dermatosis affecting the glabrous skin of the ventral abdomen and medial thighs. Clinically, flaccid bullae were accompanied by erythema, ulceration, haemorrhage and hyperpigmentation in four of six dogs; the remaining two dogs had thin skin without grossly apparent bullae. Histologically, subepidermal bullae and clefting, vascular proliferation and dilatation (phlebectasia), and alteration in the density and staining of superficial dermal collagen were seen in all dogs. In all cases, corticosteroid-containing topical products had been applied to the affected areas prior to the development of the dermatosis; skin lesions resolved when topical corticosteroids were withdrawn. Follow-up biopsy of three dogs showed resolution of the previously abnormal collagen and subepidermal clefting. Residual lesions included phlebectasia, comedones and hyperpigmentation. The authors postulate that subepidermal clefting was due to local, corticosteroid-induced skin fragility. This is the first report, to our knowledge, of bullous skin disease in dogs resulting from topical corticosteroid therapy.     

Suspected toxic shock-like syndrome in a dog with closed-cervix pyometra

Several cases of toxic shock-like syndrome (TSLS) have been reported in dogs but no inciting cause has been identified. TSLS associated with a closed-cervix pyometra was suspected in the reported bitch. The dog was evaluated for the complaint of generalized dermatopathy (erythema and oedema) and systemic signs with multiorganic involvement (depression, fever, immature neutrophilia, hypoalbuminaemia, renal disease, vomiting and diarrhoea). Histological features consistent with TSLS included superficial dermatitis with epidermal neutrophilic exocytosis and necrotic keratinocytes. The tentative diagnosis of TSLS was based on case history, clinical presentation, laboratory and histopathological findings, and the resolution of all clinical signs following surgical removal of the localized bacterial infection.     

Juvenile Pancreatic Atrophy in Greyhounds: 12 Cases (1995–2000)

Background: This study describes compound failure of the endocrine and exocrine pancreas in Greyhounds, a condition that has not been reported in the veterinary literature.
Objective: To describe the clinical and pathologic findings in 12 Greyhounds with juvenile pancreatic atrophy.
Animals: Ten Greyhounds presented for necropsy examination and 2 sibling Greyhounds presented for clinical evaluation before necropsy, all with a history of small-bowel diarrhea.
Procedures: Retrospective study of laboratory and pathologic findings in 12 Greyhounds, including serum trypsin-like immunoreactivity assays, oral glucose tolerance testing, and serum anti-insulin antibody concentrations.
Results: Gross pancreatic atrophy was found in all 12 dogs. Histopathologic lesions were found in both the endocrine and exocrine pancreas and included acinar cell apoptosis, zymogen granule loss, cytoplasmic clearing or vacuolar change, lobular atrophy, islet loss, and lymphocytic or lymphoplasmacytic pancreatitis. Antemortem test results on the 2 Greyhound puppies indicated concurrent exocrine pancreatic insufficiency (EPI) and insulin-dependent diabetes mellitus (IDDM).
Conclusions and Clinical Importance: Compound failure of the exocrine and endocrine pancreas is rarely reported in dogs and neither disease is well recognized in the Greyhound. This condition is of potential economic importance to the Greyhound racing industry.     

Diabetes mellitus-related morphoquantitative changes in the celiac ganglion neurons of the dog

Diabetes mellitus is the most common endocrine disturbance of domestic carnivores and can cause autonomic neurological disorders, although these are still poorly understood in veterinary medicine. There is little information available on the quantitative adaptation mechanisms of the sympathetic ganglia during diabetes mellitus in domestic mammals. By combining morphometric methods and NADPH-diaphorase staining (as a possible marker for nitric oxide producing neurons), type I diabetes mellitus-related morphoquantitative changes were investigated in the celiac ganglion neurons in dogs. Twelve left celiac ganglia from adult female German shepherd dogs were examined: six ganglia were from non-diabetic and six from diabetic subjects. Consistent hypertrophy of the ganglia was noted in diabetic animals with increase of 55% in length, 53% in width, and 61.5% in thickness. The ordinary microstructure of the ganglia was modified leading to an uneven distribution of the ganglionic units and a more evident distribution of axon fascicles. In contrast to non-diabetic dogs, there was a lack of NADPH-diaphorase perikarial labelling in the celiac ganglion neurons of diabetic animals. The morphometric study showed that both the neuronal and nuclear sizes were significantly larger in diabetic dogs (1.3 and 1.39 times, respectively). The profile density and area fraction of NADPH-diaphorase-reactive celiac ganglion neurons were significantly larger (1.35 and 1.48 times, respectively) in non-diabetic dogs compared to NADPH-diaphorase-non-reactive celiac ganglion neurons in diabetic dogs. Although this study suggests that diabetic neuropathy is associated with neuronal hypertrophy, controversy remains over the possibility of ongoing neuronal loss and the functional interrelationship between them. It is unclear whether neuronal hypertrophy could be a compensation mechanism for a putative neuronal loss during the diabetes mellitus.     

Serum amylase and isoamylase values in dogs with pancreatic disease

Serum amylase and isoamylase values were determined in three groups of dogs. The first group contained control dogs while the other groups contained dogs with confirmed exocrine pancreatic insufficiency and diabetes mellitus respectively. The trypsin-like immunoreactivity test was also carried out on sera from dogs with exocrine pancreatic disease (EPI). A significant difference was detected in the serum amylase values between the three groups which may be of limited diagnostic value. Dogs with EPI had values lower than normal while those with diabetes mellitus had values higher than control dogs. No evidence of exocrine pancreatic insufficiency was found in dogs with diabetes mellitus.     

Development of canine systemic lupus erythematosus model

The purpose of this study was to develop a model for canine systemic lupus erythematosus. Systemic lupus erythematosus (SLE) is a systemic autoimmune syndrome defined by clinical and serological features, including arthritis, glomerulonephritis, dermatitis and autoantibodies. SLE was induced in eight normal dogs by immunization with heparan sulphate, the major glycosaminoglycan of the glomerular basement membrane. All the heparan sulphate-immunized dogs showed mild-to-moderate levels of proteinuria and skin disease. Cutaneous signs associated with SLE including alopecia, erythema, crusting, scaling and seborrhoea were observed. Immunohistological examination of the skin lesions revealed deposition of immunoglobulin M and complement in the dermal-epidermal junction. Three of eight dogs showed lameness. The antinuclear antibody tests were positive with the antibody titres higher than 1:128. Therefore, this experimental SLE model could be useful for studying immune-mediated skin disease and autoimmunity.     

Exocrine pancreatic insufficiency as an end stage of pancreatitis in four dogs

Chronic pancreatitis is a common cause of exocrine pancreatic insufficiency (EPI) in humans and cats but is rarely recognised in dogs in which pancreatic acinar atrophy (PAA) is reportedly more common. This paper describes four dogs which developed EPI secondary to pancreatitis. Two of the dogs also had diabetes mellitus which developed before EPI. One diabetic dog had concurrent hyperadrenocorticism and was euthanased five months after presentation; the other diabetic dog died 48 months after diagnosis. The remaining dogs were alive 78 and 57 months after diagnosis. The number of affected dogs was comparable to the number of cases of presumed PAA seen over the same time period in the same institution. Chronic pancreatitis may be a more common cause of EPI in dogs than previously assumed and may be under-recognised because of difficulties in diagnosis. The relative importance of chronic pancreatitis as a cause of canine diabetes mellitus remains to be ascertained.     

Advances in canine diabetes mellitus research: etiopathology and results of islet transplantation

Histopathologic and immunocytochemical alterations in the pancreas of 18 dogs with spontaneous diabetes mellitus were evaluated. In 5 of 18 dogs (28%), extensive pancreatic damage appeared to be responsible for the development of diabetes mellitus. In the other 13 dogs, there was substantial reduction in the number of well-granulated beta cells, but the number of well-granulated alpha and delta cells was normal in 70% and 85% of the dogs, respectively. Also, insulitis lesions composed of infiltrating mononuclear cells, predominantly lymphocytes, were observed in 6 of 13 dogs (46%), but evidence of islet-directed humoral autoimmunity was not detected. Each pancreas had dense Ia (class II antigen) expression on ductal epithelia but not on islet endocrine cells. The importance of the insulitis lesions and class II antigen expression on ductal epithelial cells remains unclear. Of the 18 dogs, 8 received multidonor intrahepatic islet allografts. Allograft rejection was prevented by administration of cyclosporin. Five dogs were administered cyclosporin continuously. One dog with an allograft failed to sustain euglycemia at 231 days after transplantation, and one dog with fasting euglycemia died of pneumonia at 186 days after transplantation. In the other dogs, euglycemia was sustained for periods that ranged from 253 to 716 days.     

Definition of diabetes mellitus

The nomenclature of human diabetes mellitus (DM) has been revised, and this classification has been accepted throughout the medical world and literature. The major categories of diabetes are: insulin-dependent DM, type I or IDDM; noninsulin-dependent DM, type II or NIDDM; secondary DM or type S; impaired glucose tolerance, IGT; gestational diabetes; and previous abnormality of glucose tolerance, PrevAGT. A review of the literature has shown that over half of the documented diabetic dogs, with a single medical diagnosis, appear to be type I, IDDM, with a substantial proportion being type S, and the remainder being type II, NIDDM. Obesity is frequently associated with IGT and NIDDM. Diabetic cats most commonly have pancreatic islet destruction associated with pancreatic amyloidosis; they are insulin deficient, IDDM. The commonest causes of secondary diabetes in dogs are pancreatic damage, hyperadrenocorticism and hypersomatotropism secondary to persistent progesterone influence. Progestogen therapy is the most frequently reported cause of secondary diabetes in cats. Diabetes in horses is type S, usually secondary to a functional pituitary tumor but occasionally following chronic pancreatitis. The blood glucose ranges for normal, IGT and diabetic animals, and the normal serum insulin values of various species is tabulated.     

Dermatosis and associated systemic signs in a cat with thymoma and recently treated with an imidacloprid preparation

A cat was presented with acute-onset exfoliative erythroderma and gross and histopathological lesions of erythema multiforme. Marked cardiovascular abnormalities including heart failure occurred concurrently and a dermatogenic enteropathy was also seen. Medical treatment resolved the dermatopathy and enteropathy but the heart failure progressed. A drug reaction was initially suspected to be the underlying cause with no neoplasia being detected, but repeat radiographs subsequently revealed a thymoma which had not been visible on the initial radiographs. The dermatopathy may have been a paraneoplastic disease associated with thymoma and, possibly, exacerbated by a drug reaction to imidacloprid. The cardiovascular and gastroenterological diseases were thought to be systemic effects associated with the exfoliative erythroderma. The thymoma was surgically removed but the cat subsequently died from heart failure.     

Acute febrile neutrophilic vasculitis of the skin of young Shar-Pei dogs

Three young Shar-Pei dogs were presented for signs of an acute widespread dermatopathy associated with fever and malaise. Cutaneous lesions initially consisted of multifocal areas of skin discolouration (haemorrhagic papules, macules or plaques) or oedema, preferentially affecting the head and limbs. In some locations, pus-filled bullae were evident also. Cutaneous lesions exuded seropurulent liquid and, in time, usually progressed to full thickness necrosis and ulceration. Lesions were so widespread and severe that one of the dogs was euthanased because its owners could not afford the reconstructive surgery required to close the skin deficits left at the completion of otherwise successful therapy. Histological examination of representative biopsies showed neutrophilic dermatitis and vasculitis, which ultimately resulted in ischaemic necrosis of skin. Therapy with immunosuppressive doses of corticosteroids, and in one case cyclophosphamide, resulted in prompt amelioration of the underlying inflammatory process, although regions of skin deprived of their blood supply eventually became necrotic and sloughed. Healing occurred through granulation, contraction and epithelialisation. The physical findings in these three dogs were so similar that it is likely all suffered from the same breed-related syndrome, an immune-mediated vasculitis precipitated by some event, such as vaccination or an undetected infection. Whatever the inciting cause, it was most likely a one-off event, as the two surviving dogs were readily weaned off immunosuppressive medication without relapse.     

Vaccine-induced ischemic dermatopathy in the dog

Post-rabies vaccination alopecia associated with concurrent multifocal ischemic dermatopathy was identified in three unrelated dogs. All dogs received subcutaneous rabies vaccine dorsally between the scapulae several months prior to observation of the initial area of alopecia at the vaccination site. All three dogs developed multifocal cutaneous disease within 1–5 months after the appearance of the initial skin lesion. Cutaneous lesions were characterized clinically by variable alopecia, crusting, hyperpigmentation, erosions, and ulcers on the pinnal margins, periocular areas, skin overlying boney prominences, tip of the tail, and paw pads. Lingual erosions and ulcers were observed in two dogs. Histopathologic examination of the skin revealed moderate to severe follicular atrophy, hyalinization of collagen, vasculopathy, and cell-poor interface dermatitis and mural folliculitis. Hypovascularity was demonstrated by diminished Factor VIII staining of blood vessels. Nodular accumulations of lymphocytes, plasma cells, and histiocytes in the deep dermis and panniculus also were noted at the rabies vaccination site. An atrophic, ischemic myopathy paralleling the onset of skin disease was identified in two dogs. Histological examination of muscle biopsy specimens demonstrated perifascicular atrophy, perimysial fibrosis, and complement (C) _5b-9 (membrane attack complex) deposition in the microvasculature of both dogs with myopathy. Marked improvement of the skin disease was obtained with oral pentoxifylline and vitamin E.     

P-60 Hypercalcaemia associated with disseminated Lagenidium spp. infection in a dog: case report

Opportunistic dermatoses can occur in case of immunosuppressive diseases. The first case was a 12-year-old domestic short-haired cat suffering from diabetes with a phaeohyphomycosis due to Scytalidium spp. associated with cutaneous hemangiosarcoma. A painless and ulcerated nodule was observed on a digit with fistulous tracts over the metatarsal joint. Histopathological examination of the nodule revealed a hemangiosarcoma in which brownish fungal colonies were found. Itraconazole (5 mg/kg twice daily), then amputation, allowed 12 months of survival (pulmonary metastases). The second case concerned a 13-year-old Siamese cat with cheyletiellosis associated with spontaneous Cushing's disease and diabetes mellitus. This cat exhibited scales and miliary dermatitis on the trunk associated with polyuria, polydipsia and a pot-belly. Acetate tape impression showed Cheyletiella blakei mites and eggs. Blood analysis revealed diabetes mellitus and spontaneous hyperadrenocorticism. The owner refused treatment. The third case was a 14-year-old domestic short-haired cat with generalized demodicosis associated with iatrogenic Cushing's disease and diabetes mellitus. Long-acting glucocorticoids had been used for treatment of plasma cell stomatitis for 5 years. This cat exhibited erythema, scales, self-induced alopecia, thin skin and moderate pruritus associated with polyuria and polydipsia. Cutaneous lesions principally developed on the abdomen and flanks. Skin scrapings and trichogram showed numerous Demodex cati mites. Routine blood work demonstrated diabetes mellitus and iatrogenic Cushing's disease. Treatment was based on insulin therapy, milbemycin oxime (1 mg/kg once daily) and chlorambucil (0.2 mg/kg once daily). The demodicosis was cured after 4 months, but the cat died of cutaneous and ocular herpesvirus infection 10 months later.
Funding: Self-funded.     

Retrospective evaluation of urinary tract infection in 42 dogs with hyperadrenocorticism or diabetes mellitus or both

A retrospective study was performed to determine the proportion of dogs with hyperadrenocorticism or diabetes mellitus or both that had urinary tract infection (UTI) and to describe clinical and laboratory findings. Dogs with these endocrine disorders were included if results of quantitative urine culture were available and dogs were not receiving antimicrobials. Dogs with positive urine cultures were considered to have UTI and dogs with negative urine cultures were used as controls. Information including history, clinical signs, physical examination findings, and results of laboratory tests and urine culture was extracted from all records. Findings in dogs with UTI were compared with control dogs. There were 101 dogs with hyperadrenocorticism or diabetes mellitus or both that met inclusion criteria; 42 (41.6%) had UTI and 59 (58.4%) did not. UTI was present in 46% of dogs with hyperadrenocorticism, 37% of dogs with diabetes mellitus, and 50% of dogs with both endocrine disorders. There was no association between endocrine group and occurrence of UTI. Escherichia coli was the most common bacteria isolated, and cultures from 29 dogs (69%) showed growth of this organism. Of dogs with UTI, <5% had stranguria, pollakiuria, or discolored urine, whereas 60% had pyuria and 69% had bacteriuria. We conclude that UTIs are common in dogs with hyperadrenocorticism, diabetes mellitus, or both diseases. Clinical signs of UTI, however, are uncommon and results of urinalysis may be normal. Therefore, it is appropriate to recommend urine culture as part of the evaluation of dogs with these endocrine disorders.