Aflatoxicosis in nine dogs after exposure to contaminated commercial dog food.

The purpose of this study was to characterize light and electron microscopic findings from 9 dogs that had consumed aflatoxin-contaminated commercial dog food from recalled batches. Four dogs died and 5 were euthanized after signs of liver failure. Analysis of feed and liver samples confirmed exposure to aflatoxin. Of the 9 dogs, 8 had classic signs of liver failure, and 1 had signs of liver failure. Enlarged, pale yellow livers were seen macroscopically at necropsy in the dogs with subacute hepatopathy, and cirrhosis was noted in the dog with chronic hepatopathy. Histopathologic findings included hepatic lipidosis, portal fibroplasia, and biliary hyperplasia, which supported a diagnosis of subacute toxic hepatopathy in the 8 symptomatic animals. Marked lobular atrophy, bridging portal fibrosis, and regenerative hepatocellular nodules characterized the dog with chronic hepatopathy. Electron microscopy revealed marked hepatocellular lipid vacuolation and early fibroplasia in the dogs with acute hepatopathy and marked fibrosis and regeneration in the dog with chronic hepatopathy. Analysis of feed for aflatoxin consistently revealed high levels of aflatoxin B1 (range of 223-579 ppb), and hepatic tissue contained elevated levels of aflatoxin B1 metabolite M1 (0.6-4.4 ppb). Although dogs are not commonly affected by aflatoxicosis, they are highly susceptible and can present with classic signs of acute or chronic hepatopathy. Characteristic gross, histologic, and electron microscopic changes help pathologists determine a presumptive toxic insult. Detecting aflatoxins or their metabolites in feed or liver specimens can help confirm the diagnosis of aflatoxicosis.     

Panniculitis associated with pancreatic necrosis in a dog

A seven-year-old male labrador cross was presented with lethargy, pyrexia and multiple nonpruritic draining skin lesions. The dog had sterile nodular panniculitis which, at necropsy, was found to be associated with a bile duct carcinoma leading to pancreatic necrosis.     

Renal medullary crest necrosis associated with phenylbutazone therapy in horses

Thirty-five cases of renal medullary crest necrosis morphologically similar to the renal papillary necrosis of analgesic nephropathy as described in man and rats are reported in horses receiving maintenance dosages of phenylbutazone. The primary lesion is a well-demarcated focal medullary necrosis resulting in sequestration of fragments of the renal crest. Renal cortical lesions are considered secondary to the medullary necrosis and consist of segmental pallor as a result of tubular dilatation, filtrate retention, and interstitial edema. Ischemia in concert with phenylbutazone is suggested as the etiology. Renal medullary crest necrosis is presented as more appropriate morphological terminology for this lesion in the equine species than renal papillary necrosis as is used in man and rats.     

Nephrogenic diabetes insipidus in a dog with renal medullary lesions.

Antidiuretic hormone (ADH) administration to a polyuric Miniature Poodle did not alter diuresis. Plasma ADH concentrations were high, and urine osmolality remained low during water deprivation. From these findings, it was concluded that the polyuria was of renal origin. In addition, the glomerular filtration rate was found to be high. Electron microscopic examination of the renal medulla revealed vacuoles containing myelinic figures and fingerprint structures in the cells of the Henle loops, blood vessels, and interstitium, similar to those in lysosomal lipid storage disease. Their absence in collecting duct epithelium indicated that the defect in concentrating ability was due to a disturbance of the counter-current multiplier mechanism rather than to a defect in ADH receptors.     

Polycythemia associated with renal fibrosarcoma in a dog

A 10-year-old Beagle-type dog with intermittent vomiting and anorexia had an absolute polycythemic condition. A renal mass was detected and removed by total nephrectomy. After surgery, the hematologic values returned to normal, suggesting that the tumor was the cause of the polycythemia. The histologic diagnosis was fibrosarcoma. In dogs, secondary polycythemia has otherwise been reported with renal carcinoma and lymphosarcoma.     

Thrombo-ischaemic pinnal necrosis associated with fenbendazole treatment in a dog

An 11-week-old, female West Highland white terrier was presented with necrosis of the distal third of both pinnae. Haematology, biochemistry and urinalysis, Coombs test, antinuclear antibody and cold autoagglutinin antibody tests were normal. A drug reaction to fenbendazole was diagnosed. The necrotic ear tips were surgically removed. Histopathology revealed extensive coagulative necrosis of the epidermis and superficial to mid-dermis, a moderate interstitial neutrophilic infiltrate and complete thrombotic occlusion and necrosis of blood vessels. There was also endothelial cell activation and proliferation with endothelial cell cushions protruding into the vascular lumen. Immunohistochemistry for factor VIII-related antigen confirmed endothelial cell involvement. This case represents an unusual, drug-induced, thrombo-ischaemic necrosis of the pinnae. It is also, to the authors' knowledge, the first report of fenbendazole sensitivity in a dog. The histopathology is similar to previous cases of proliferative thrombovascular pinnal necrosis, suggesting that drug reactions should be considered in this condition.     

Dermal necrosis associated with Rocky Mountain spotted fever in four dogs

Four dogs with Rocky Mountain spotted fever developed extensive dermal necrosis. Factors contributing to this complication included delay in initiation of appropriate therapy.     

Isoniazid-induced seizures with secondary rhabdomyolysis and associated acute renal failure in a dog

Isoniazid-induced seizures resulted in rhabdomyolysis and associated acute renal tubular necrosis in a dog. Rhabdomyolysis and myoglobinuric renal failure, although recognised in the dog, are reported infrequently as a consequence of seizures. The clinical presentation of isoniazid toxicity in a dog is described.     

Acute renal failure associated with contrast medium administration in a dog.

Intravenous administration of an ionic radiographic contrast medium was believed to have caused acute oliguric renal failure in a young dog. Intravenous pyelography was done on a healthy 14-month-old female Lhasa Apso prior to reconstructive surgery for pseudohermaphroditism. Within 24 hours of the radiographic procedure, acute oliguric renal failure developed. Cause for the renal failure was not found other than the recent IV administration of radiographic contrast medium. Treatment with fluids, furosemide, and dopamine was successful in returning renal function to normal. Various adverse reactions to IV administration of contrast media in human beings and animals have been reported; however, to our knowledge, acute renal dysfunction induced by IV administration of contrast material has not been reported in dogs.     

Hypertrophic osteopathy associated with renal pelvis transitional cell carcinoma in a dog

A 6-year-old male, Belgian shepherd dog was presented with lethargy, oliguria, hematuria, and reluctance to move. The dog developed hypertrophic osteopathy secondary to renal pelvis transitional cell carcinoma. A nephrectomy was performed and after a year, the dog was completely asymptomatic, and no evidence of metastatic disease was present.     

Metabolic epidermal necrosis in a dog associated with pancreatic adenocarcinoma, hyperglucagonaemia, hyperinsulinaemia and hypoaminoacidaemia

A case of metabolic epidermal necrosis associated with a pancreatic carcinoma is described. Normoglycaemia, reduced serum fructosamine, and hypoaminoacidaemia were identified. Hyperinsulinaemia and hyperglucagonaemia were documented. Immunohistochemistry documented strong tumour expression of both insulin and glucagon supporting combined paraneoplastic production of both hormones by the tumour. Enteral protein and fatty acid supplementation and parenteral amino acid supplementation proved ineffective. Metastasis to regional lymph nodes was identified and the patient was euthanased.     

Renal allograft histopathology in dog leukocyte antigen mismatched dogs after renal transplantation

OBJECTIVE: To evaluate allograft histopathology in dog leukocyte antigen (DLA)-mismatched dogs undergoing renal transplantation, with transient immunosuppression. STUDY DESIGN: Prospective study. ANIMALS: Ten healthy adult mongrel dogs. METHODS: Reciprocal renal transplantation and bilateral nephrectomy were performed. Immune conditioning consisted of nonmyeloablative (200 cGy), total body irradiation (TBI), bone marrow transplantation (BMT; 7 dogs), cyclosporine (CSA; 15 mg/kg every 12 hours), mycophenolate mofetil (MMF; 10 mg/kg every 12 hours) and intermittent prednisone (1 mg/kg every 12-24 hours). Biopsies were collected at transplantation, during full immunosuppression (44-90 days), and once medications were reduced or discontinued (228-580 days). Biopsies were evaluated for interstitial, tubular, vascular, and glomerular lesions. Blood urea nitrogen, creatinine, serum CSA concentrations, and clinical score were determined at each biopsy. RESULTS: Seven dogs survived >200 days (mean, 380 days). Transient CSA toxicity was suspected in 6 dogs. Lymphocytic, plasmacytic interstitial inflammation, and tubulitis progressed when immunosuppressive medications were decreased. All 7 dogs had histologic lesions consistent with some degree of allograft rejection at study end. CONCLUSION: Nonmyeloablative TBI, BMT, and short-term immunosuppression with CSA, MMF, and prednisone allowed renal allograft function and dog survival for >200 days. It appears unlikely that total drug withdrawal will be possible in unrelated DLA-mismatched dogs using this protocol. CLINICAL RELEVANCE: Transient immunosuppression with MMF, CSA, and prednisone along with BMT and nonmyeloablative TBI may make kidney transplantation a clinical reality for treatment of kidney failure in dogs. Initiating both MMF and CSA at lower dosages may potentially eliminate early renal allograft injury.     

Use of capecitabine after renal allograft transplantation in dog erythrocyte antigen-matched dogs

OBJECTIVES: To investigate the use of a capecitabine (CAP)-based regimen after renal transplantation in dogs. STUDY DESIGN: Prospective, pilot study. ANIMALS: Healthy, unrelated, dog erythrocyte antigen (DEA)-matched, adult beagles. METHOD: Standard heterotopic renal transplantation with native nephrectomy was performed in 7 dogs. Dogs received oral, twice daily, CAP (250 mg/m2), cyclosporine-A (CsA) (4 mg/kg), ketoconazole (5 mg/kg), and prednisolone (0.25 mg/kg). After 90 days the surviving dogs were euthanatized and complete necropsy was performed. RESULTS: Seven transplants were performed. All dogs survived surgery. Six dogs had acute neurotoxicity, which resulted in death or euthanasia of 2 dogs within 2 days of surgery. In the remaining dogs, toxicity resolved rapidly with cessation of drug administration. Thereafter, modification of the regimen minimized toxicity. The 5 remaining dogs survived to study end; 4 dogs had no evidence of graft rejection. Necropsy examination was mostly unremarkable in all dogs. There were no major changes in CBC or biochemical values, except for a significant increase in serum calcium. CONCLUSIONS: CAP appeared well tolerated in most dogs. Toxicity occurred but abated with modification of the drug regimen. Efficacy for postoperative immunosuppression cannot be determined by this study, although results are promising. CLINICAL RELEVANCE: CAP-CsA-prednisolone is an effective, oral immunosuppressive regimen for prevention of acute allograft rejection in DEA-matched beagles. Further studies on dose, toxicity, and efficacy compared with current immunosuppressive regimens are needed before use in clinical practice.     

Nodular dermatofibrosis and cystic renal disease in three mixed-breed dogs and a Boxer dog

Three mixed-breed dogs and a Boxer dog with nodular dermatofibrosis are described. The three mixed breed dogs had concurrent renal epithelial cysts ( n  = 2) or renal cystadenomas ( n  = 1); these lesions were visualized antemortem on ultrasonographic examination. One of these dogs was a 7-year-old Labrador Retriever-Gordon Setter mixed breed which survived 5 years after diagnosis, and was euthanized for unrelated causes. The Boxer dog had renal cystic adenomatous hyperplasia and renal cystadenocarcinomas which were not visualized on ultrasonographic examination but were diagnosed at necropsy.