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Spontaneous hyperlipidemia in rats causes glomerular disease. Idiopathic hypertriglyceridemia (HTG) is prevalent in Miniature Schnauzers, but its relationship with proteinuria is unknown. Decreased activity of major lipid metabolism enzymes, lipoprotein lipase (LPL) and hepatic lipase (HL), may play a role in the cyclic relationship between hyperlipidemia and proteinuria. These enzymes have also not been previously investigated in Miniature Schnauzers. The aims of this study were to determine the relationship between HTG and proteinuria in Miniature Schnauzers and to measure LPL and HL activities in a subset of dogs. Fifty-seven Miniature Schnauzers were recruited (34 with and 23 without HTG). Fasting serum triglyceride concentrations and urine protein-to-creatinine ratios (UPC) were measured in all dogs, and LPL and HL activities were determined in 17 dogs (8 with and 9 without HTG). There was a strong positive correlation between triglyceride concentration and UPC (r = 0.77-0.83, P

A 7 mo old intact female golden retriever was evaluated for acute vomiting. Abdominal radiographs revealed a possible gastric foreign body. Upper gastrointestinal endoscopy revealed an edematous, tubular antral mass, which on further evaluation was determined to be a pylorogastric intussusception based on radiographic, endoscopic, and surgical findings. Spontaneous resolution of the intussusception occurred upon surgical exploration of the abdomen. Histopathology of a full-thickness gastric biopsy revealed vascular congestion consistent with an intussusception, but did not indicate the primary cause. The dog recovered uneventfully from surgery and had no further vomiting during the 6 mo follow-up period. This case was significant as it was the first report of pylorogastric intussusception diagnosed using endoscopy. This description of the unique endoscopic appearance of pylorogastric intussusception will be useful for the veterinary endoscopist.

A dog presenting for chronic purulent nasal discharge was diagnosed with an Eucoleus boehmi infection based upon rhinoscopic appearance of the nasal worms in situ, identification of the adult parasites in rhinoscopic nasal biopsies, and ova in the feces. The dog was successfully treated with a 2 wk course of fenbendazole and measures preventing reinfection through coprophagia. Patients with chronic nasal discharge should have a fecal examination performed to rule out infection with E. boehmi.

V itamin D deficiency is the leading cause of rickets in growing llamas and alpacas in North America, New Zealand, and Australia. Prophylactic treatment with vitamin D supplements is a common husbandry practice in North America. This case report describes the clinical course, diagnostics, and pathological findings in 2 alpaca cria (Vicugna pacos), presenting at 18 days and 8 days of age, with presumptive vitamin D intoxication. Both cria developed tissue mineralization and acute renal failure after administration of excessive doses of vitamin D. Presentation of camelids with a history of vitamin D administration associated with hypercalcemia, hyperphosphatemia, and renal dysfunction strongly suggests vitamin D intoxication. Early recognition of these signs can improve clinical outcomes.

Gastrointestinal endoscopy is a minimally invasive diagnostic tool for cats and dogs with signs of gastrointestinal disease. This retrospective study examined the case records of six cats and one dog diagnosed with perforation secondary to gastrointestinal endoscopy. Gastrointestinal perforation occurred in 1.6% of cats and 0.1% of dogs that underwent endoscopy during the 17 yr study period (from 1993 to 2010). It can be difficult to predict what animals are at risk for gastrointestinal perforation but possible risk factors suggested by this study include small intestinal infiltrative disease in cats and preexisting gastrointestinal ulceration in both cats and dogs. Overall, gastrointestinal endoscopy is associated with a low rate of gastrointestinal perforation.

Physaloptera infections were diagnosed endoscopically in 18 dogs. Each case had vomiting as the primary clinical sign, and four cases had regurgitation as a concurrent sign. Fecal flotations, using magnesium sulfate solution, were performed in 12 of the 18 cases and were negative for Physaloptera eggs. In 12 of the 18 cases, only one worm was seen during endoscopic examination. Fifteen of 18 cases were treated with pyrantel pamoate, and 10 of 12 cases with follow-up had resolution of their vomiting.

Two diabetic dogs were presented for anorexia, persistent fever, and poor control of hyperglycemia. Both had neutrophilia with left shift, hypoalbuminemia, and increased serum alkaline phosphatase (SAP) activity. Radiography indicated intrahepatic gas densities in 1 dog and a hepatic mass in the other. Abdominal sonography demonstrated multiple well-demarcated hypoechoic hepatic lesions consistent with abscesses. Both dogs were successfully treated by surgical resection of the abscessed liver lobes in conjunction with antibiotics and supportive therapy. Good control of hyperglycemia was achieved in both dogs after recovery. Intracellular and extracellular Gram-negative rod-shaped bacteria were abundant in the abscesses from both dogs. These cases suggest an association between diabetes mellitus and hepatic abscessation.

Canine histiocytic ulcerative colitis (HUC) is characterized by colonic inflammation with predominantly periodic acid-Schiff (PAS)-positive macrophages. The inflammation results in colonic thickening, ulcerations, and distortion of normal glandular architecture. Resultant clinical signs consist of chronic large bowel diarrhea, tenesmus, and marked weight loss, and the disease frequently results in euthanasia. Conventional therapy consists of some combination of prednisone, azathioprine, sulfasalazine, and metronidazole. Nine dogs (8 Boxers and 1 English Bulldog) with histologic confirmation of HUC were treated with antibiotic therapy (either with enrofloxacin alone or in combination with metronidazole and amoxicillin). Clinical signs, physical examination findings, laboratory abnormalities, and the histologic severity of the disease were evaluated. Four of the 9 dogs had been treated previously with conventional therapy and had failed to respond favorably; then, these dogs were placed on antibiotic therapy (enrofloxacin, n = 1; enrofloxacin, metronidazole, and amoxicillin, n = 3) and had resolution of clinical signs within 3-12 days. Five dogs were treated solely with antibiotic therapy (enrofloxacin, n = 1; enrofloxacin and metronidazole, n = 1; enrofloxacin, metronidazole, and amoxicillin, n = 3), and clinical signs resolved in 2-7 days. Repeated biopsy specimens were obtained from 5 dogs after treatment, and all showed marked histologic improvement. The increase in body weight after treatment was statistically significant (P = .01). Three dogs currently are not on any treatment and have had resolution of clinical signs for up to 14 months. These observations suggest that an infectious agent responsive to antibiotics plays an integral role in the clinical manifestation of canine HUC, and they support the use of antibiotics in its treatment.

Benign esophageal strictures in 6 cats and 7 dogs were treated with endoscopically guided balloon dilatation. Six of 13 had a history of anesthesia within 3 weeks prior to the onset of signs; 8 animals had a single stricture, and 5 had multiple strictures, for a total of 19 strictures. Four of the 19 strictures were in the upper esophagus, 11 were in the middle esophagus, and 4 were in the lower esophagus. The luminal diameters ranged from 1 to 18 mm, with a mean of 5.1 mm. Twelve animals survived the immediate postprocedure period and had a total of 50 dilatation procedures performed; the mean number of procedures per animal was 4.2 (range, 2 to 8). Complications included mild bleeding and tearing (11 of 13), moderate bleeding (1 of 13), and esophageal perforation (1 of 13). The cat with the perforation was subsequently euthanized. Follow-up information was available on the 12 remaining animals; 9 were known to be alive 6 to 59 months (mean, 28.2 months) after dilatation. Two were euthanized, 1 for persistence of signs and the other for unrelated causes. One animal died of possible aspiration pneumonia. Three of 13 animals had complete and 9 had partial resolution of signs. Of the 9 animals with partial resolution, 7 were substantially better with dietary modification, 1 was moderately better, and 1 had minimal improvement. Eleven of 13 animals (85%) had a successful outcome with moderate to complete resolution of signs. Thus, it is concluded that endoscopically guided balloon dilatation is an effective and relatively safe treatment for benign esophageal strictures in dogs and cats.

Acute hepatic failure is characterized by a sudden catastrophic compromise of hepatic failure that causes clinical signs such as anorexia, depression, vomiting, diarrhea, icterus, and encephalopathy. Injurious hepatotoxins, drugs, infectious agents, or metabolic disturbances can cause acute hepatic failure; however, in many cases, the inciting cause is not determined. Treatment is aimed at controlling complications such as fluid-electrolyte imbalances, hepatic encephalopathy, hypoglycemia, bleeding diathesis, gastric ulcer, sepsis, and endotoxemia, in order to provide time for liver regeneration and recovery.

In order to evaluate the enteropancreatic hormone axis in dogs with pancreatic acinar atrophy, we measured the release of gastric inhibitory polypeptide and pancreatic polypeptide in response to a standard meal and a meal containing pancreatic enzymes in affected dogs and controls. Postprandial release of pancreatic polypeptide was normal in dogs with pancreatic atrophy and was not affected by addition of pancreatic enzymes to the food. Gastric inhibitory polypeptide was not released after a standard meal in affected dogs, but this blunted response was corrected by the addition of pancreatic enzymes to the food. Feeding the enzyme alone did not stimulate a gastric inhibitory polypeptide response. These results, in part, support similar observations previously reported in children with exocrine pancreatic insufficiency associated with cystic fibrosis. We conclude that dogs with idiopathic pancreatic acinar atrophy can be used as an animal model for future study of enteropancreatic hormonal abnormalities that occur in human beings with exocrine pancreatic insufficiency.

The diagnosis and management of the chronic bronchitis patient can be a challenging, but rewarding, task for the veterinarian. The normal respiratory defense mechanisms and the pathophysiologic responses to the pathologic changes are of dramatic importance in understanding the choices of therapy. The keys to successful management of the patient lie in correct assessment of the clinical features and diagnostic procedures and periodic reevaluation of the patient's response to therapy and age/environment-related progression of pathology. Lastly, the clinician must create a realistic attitude for the owner regarding chronically diseased patients.