Robert G. Sherding

Antibiotic‐Responsive Histiocytic Ulcerative Colitis in 9 Dogs

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.

Acute renal failure and anuria associated with vitamin D intoxication in two alpaca (Vicugna pacos) cria.

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.

Rhinoscopic Diagnosis of Eucoleus boehmi Infection in a Dog

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.

Postprandial release of gastric inhibitory polypeptide (GIP) and pancreatic polypeptide in dogs with pancreatic acinar atrophy: Correction of blunted GIP response by addition of pancreatic enzymes to a meal

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.

Effects of Zinc‐l‐Carnosine and Vitamin E on Aspirin‐Induced Gastroduodenal Injury in Dogs

BACKGROUND Nonsteroidal anti-inflammatory drugs frequently cause gastrointestinal (GI) injury. Zinc-L-carnosine has antioxidant, anti-inflammatory, mucosal protective, and healing properties in rodent models and in some human studies of GI injury. HYPOTHESIS The combination of zinc-L-carnosine and vitamin E attenuates aspirin-induced gastroduodenal mucosal injury. ANIMALS Eighteen healthy random-source Foxhound dogs. METHODS In this randomized, double-blinded, placebo-controlled study dogs were treated with placebo (n = 6; 0X group), 30 mg/30 IU (n = 6; 1X group), or 60 mg/60 IU (n = 6; 2X group) zinc-L-carnosine/vitamin E orally every 12 hours for 35 days. Between Day 7 and 35, GI mucosal lesions were induced with aspirin (25 mg/kg p.o. q8h). Mucosal injury lesions (hemorrhage, erosion, and ulcer) were assessed by gastroduodenoscopy on Days 14, 21, and 35 with a 12-point scoring scale. RESULTS At baseline (Day -1) gastroscopy scores were not significantly different between groups (mean ± SD: 0X, 4.4 ± 0.8; group 1X, 4.4 ± 0.6; group 2X, 4.2 ± 0.3; P= .55). Gastroscopy scores increased significantly in all groups between Day -1 and Days 14, 21, and 35 (P < .0001). On Day 35, gastroscopy scores were 29.2 ± 5.2 (0X), 27.3 ± 3.7 (1X), and 28.6 ± 3.3 (2X). Mean gastroscopy scores were not significantly different among treatment groups on any of the days (P = .61). CONCLUSIONS AND CLINICAL IMPORTANCE Administration of the combination of zinc-L-carnosine and vitamin E at 1X or 2X dosing did not attenuate aspirin-induced gastroduodenal mucosal injury.

Physaloptera infection in 18 dogs with intermittent vomiting

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.

Endoscopic Diagnosis of a Pylorogastric Intussusception with Spontaneous ResolutionS

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.

Gastrointestinal Perforation Associated With Endoscopy in Cats and Dogs

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.