The mucosa-associated microflora is increasingly considered to play a pivotal role in the pathogenesis of inflammatory bowel disease. This study explored the possibility that an abnormal mucosal flora is involved in the etiopathogenesis of granulomatous colitis of Boxer dogs (GCB). Colonic biopsy samples from affected dogs (n ‫؍‬ 13) and controls (n ‫؍‬ 38) were examined by fluorescent in situ hybridization (FISH) with a eubacterial 16S rRNA probe. Culture, 16S ribosomal DNA sequencing, and histochemistry were used to guide subsequent FISH. GCB-associated Escherichia coli isolates were evaluated for their ability to invade and persist in cultured epithelial cells and macrophages as well as for serotype, phylogenetic group, genome size, overall genotype, and presence of virulence genes. Intramucosal gram-negative coccobacilli were present in 100% of GCB samples but not controls. Invasive bacteria hybridized with FISH probes to E. coli. Three of four GCB-associated E. coli isolates adhered to, invaded, and replicated within cultured epithelial cells. Invasion triggered a "splash"-type response, was decreased by cytochalasin D, genistein, colchicine, and wortmannin, and paralleled the behavior of the Crohn's disease-associated strain E. coli LF 82. GCB E. coli and LF 82 were diverse in serotype and overall genotype but similar in phylogeny (B2 and D), in virulence gene profiles (fyuA, irp1, irp2, chuA, fepC, ibeA, kpsMII, iss), in having a larger genome size than commensal E. coli, and in the presence of novel multilocus sequence types. We conclude that GCB is associated with selective intramucosal colonization by E. coli. E. coli strains associated with GCB and Crohn's disease have an adherent and invasive phenotype and novel multilocus sequence types and resemble E. coli associated with extraintestinal disease in phylogeny and virulence gene profile.

The inherent heterogeneity of bone cells complicates the interpretation of microarray studies designed to identify genes highly associated with osteoblast differentiation. To overcome this problem, we have utilized Col1a1 promoter-green fluorescent protein transgenic mouse lines to isolate bone cells at distinct stages of osteoprogenitor maturation. Comparison of gene expression patterns from unsorted or isolated sorted bone cell populations at days 7 and 17 of calvarial cultures revealed an increased specificity regarding which genes are selectively expressed in a subset of bone cell types during differentiation. Furthermore, distinctly different patterns of gene expression associated with major signaling pathways (Igf1, Bmp, and Wnt) were observed at different levels of maturation. Some of our data differ from current models of osteoprogenitor cell differentiation and emphasize components of the pathways that were not revealed in studies based on a total cell population. Thus, applying methods to generate more homogeneous populations of cells at a defined level of cellular differentiation from a primary osteogenic culture is feasible and leads to a novel interpretation of the gene expression associated with increasing levels of osteoprogenitor maturation.

RSV-related hospitalization creates significant distress for infants and children, caregivers, and families, with some effects extending as long as 60 days after discharge.

The records of 23 dogs and cats diagnosed with spontaneous gastroduodenal perforation (GDP) were retrospectively reviewed. Survival was 63% in dogs and 14% in cats. Rottweilers <5 years of age were overrepresented. Clinical evidence of gastrointestinal bleeding was common in dogs but not in cats. Shock was an uncommon presenting condition in dogs and was not closely linked to outcome. In fact, progression of an ulcerating lesion to GDP was not associated with marked changes in symptoms exhibited by many patients in this study. Most GDPs were associated with histopathological evidence of subacute or chronic peritoneal reaction at the time of diagnosis. This suggests that diagnostic methods employed lacked sensitivity in identifying early perforating lesions, and that dramatic signs of acute abdomen following gastroduodenal perforation may not be as common as was previously thought.

The ante mortem detection of pancreatitis in four cats is reported. Clinical findings included vomiting, lethargy and constipation in all the cats, diabetes mellitus in two cats and severe jaundice and a vitamin K responsive coagulopathy in one cat. Serum amylase was normal in all the cats and serum lipase was elevated in one azotaemic cat. Ultrasonography revealed predominantly hypoechoic masses in the right cranial quandrant of the abdomen of each cat. The anatomical location of these masses was consistent with the pancreas. Gross examination supported these ultrasonographic observations. The pancreatic lesions were characterised histologically as acute necrotising pancreatitis, acute necrotising pancreatitis with abscessation, chronic active pancreatitis with cystic dilatation of the pancreatic duct causing bile duct obstruction and chronic active pancreatitis with nodular hyperplasia. This report indicates that pancreatitis is a clinically significant disease in cats that may be diagnosed ante mortem.

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.

The clinical signs, clinicopathologic test results, portal pressure, and gross appearance of the liver of dogs with idiopathic noncirrhotic portal hypertension may be identical to those of dogs with cirrhosis; therefore liver biopsy is crucial. Because the prognosis for idiopathic noncirrhotic portal hypertension is generally favorable, owners of affected dogs should be discouraged from choosing euthanasia.

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 ϭ 1; enrofloxacin, metronidazole, and amoxicillin, n ϭ 3) and had resolution of clinical signs within 3-12 days. Five dogs were treated solely with antibiotic therapy (enrofloxacin, n ϭ 1; enrofloxacin and metronidazole, n ϭ 1; enrofloxacin, metronidazole, and amoxicillin, n ϭ 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 ϭ .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.