Hypothesis: Certain variables that are routinely measured during the diagnostic evaluation of dogs with chronic enteropathies will be predictive for outcome and a new clinical disease activity index incorporating these variables can be applied to predict outcome of disease.Animals: Seventy dogs were entered into a sequential treatment trial with elimination diet (FR, food-responsive group) followed by immunosuppressive treatment with steroids if no response was seen with the dietary trial alone (ST, steroidtreatment group). A 3rd group consisted of dogs with panhypoproteinemia and ascites (PLE, protein-losing enteropathy) that were treated with immunosuppressive doses of steroids.Methods: Three years of follow-up information was available for all dogs. Clinicopathologic variables were tested for their ability to predict negative outcome, defined as euthanasia due to refractoriness to treatment. Different scoring systems including different combinations of these variables were evaluated using receiver operating characteristic (ROC) curves.Results: Thirteen of 70 (18%) dogs were euthanized because of intractable disease. Univariate analysis identified a high clinical activity index, high endoscopic score in the duodenum, hypocobalaminemia (,200 ng/L) and hypoalbuminemia (,20 g/L) as risk factors for negative outcome.Conclusions and clinical importance: Based on the factors identified by logistic regression and ROC curve analysis, a new clinical scoring index (CCECAI) was defined that predicts negative outcome in dogs suffering from chronic enteropathies.

Hypothesis: Certain variables that are routinely measured during the diagnostic evaluation of dogs with chronic enteropathies will be predictive for outcome and a new clinical disease activity index incorporating these variables can be applied to predict outcome of disease. Animals: Seventy dogs were entered into a sequential treatment trial with elimination diet (FR, food-responsive group) followed by immunosuppressive treatment with steroids if no response was seen with the dietary trial alone (ST, steroid-treatment group). A 3rd group consisted of dogs with panhypoproteinemia and ascites (PLE, protein-losing enteropathy) that were treated with immunosuppressive doses of steroids. Methods: Three years of follow-up information was available for all dogs. Clinicopathologic variables were tested for their ability to predict negative outcome, defined as euthanasia due to refractoriness to treatment. Different scoring systems including different combinations of these variables were evaluated using receiver operating characteristic (ROC) curves. Results: Thirteen of 70 (18%) dogs were euthanized because of intractable disease. Univariate analysis identified a high clinical activity index, high endoscopic score in the duodenum, hypocobalaminemia (,200 ng/L) and hypoalbuminemia (,20 g/L) as risk factors for negative outcome. Conclusions and clinical importance: Based on the factors identified by logistic regression and ROC curve analysis, a new clinical scoring index (CCECAI) was defined that predicts negative outcome in dogs suffering from chronic enteropathies.

Baseline information for SSI surveillance in our hospital and for comparison with other studies was defined. The factors identified may help to predict infections in surgical patients and to take adequate preventive measures for patients at risk.

Background: Metronidazole has a substantial impact on the gut microbiome. However, the recovery of the microbiome after discontinuation of administration, and the metabolic consequences of such alterations have not been investigated to date. Objectives: To describe the impact of 14-day metronidazole administration, alone or in combination with a hydrolyzed protein diet, on fecal microbiome, metabolome, bile acids (BAs), and lactate production, and on serum metabolome in healthy dogs. Animals: Twenty-four healthy pet dogs. Methods: Prospective, nonrandomized controlled study. Dogs fed various commercial diets were divided in 3 groups: control group (no intervention, G1); group receiving hydrolyzed protein diet, followed by metronidazole administration (G2); and group receiving metronidazole only (G3). Microbiome composition was evaluated with sequencing of 16S rRNA genes and quantitative polymerase chain reaction (qPCR)-based dysbiosis index. Untargeted metabolomics analysis of fecal and serum samples was performed, followed by targeted assays for fecal BAs and lactate. Results: No changes were observed in G1, or G2 during diet change. Metronidazole significantly changed microbiome composition in G2 and G3, including decreases in richness (P < .001) and in key bacteria such as Fusobacteria (q < 0.001) that did not fully resolve 4 weeks after metronidazole discontinuation. Fecal dysbiosis index was significantly increased (P < .001). Those changes were accompanied by increased fecal total lactate (P < .001), and decreased secondary BAs deoxycholic acid and lithocholic acid (P < .001).

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Background: Histopathology is widely used for the diagnosis of inflammatory bowel disease in dogs. Variations in lesions and unavailability of uniform grading systems limit the usefulness of histologic examination. Hypothesis: CD3 cell numbers in chronic enteropathies of dogs correlate with clinical activity of the disease and with severity of histopathologic changes. Animals: Nineteen client‐owned dogs examined because of chronic diarrhea, vomiting, or both. Methods: Samples of duodenal and colonic mucosa were collected endoscopically before and after treatment. Dogs that responded to a hypoallergenic diet were grouped as food‐responsive diarrhea dogs (FRD, n = 10). Dogs with no clinical improvement after 10 days of treatment then received prednisolone (immunosuppressive doses) and were grouped as steroid‐responsive diarrhea dogs (SRD, n = 9). Histopathologic assessment with a standardized grading system was performed retrospectively on the intestinal samples. Histologic score, total number of infiltrating cells, and CD3‐positive cells were counted and compared with the clinical scoring. Results: No statistically significant difference was detected among histologic grading, total number of cells in the lamina propria, and T‐cell numbers in biopsies before and after treatment in either group (FRD and SRD). Conclusions and Clinical Importance: Currently used histopathologic grading scores, total numbers of cells, and numbers of CD3‐positive cells did not allow differentiation between FRD and SRD and did not correlate with clinical response to therapy. Based on these results, new grading scores assessing other criteria than total cell numbers and CD3‐positive cells should be evaluated in the future.

We evaluated whether a probiotic supplementation in dogs with food responsive diarrhoea (FRD) has beneficial effects on intestinal cytokine patterns and on microbiota. Twenty-one client-owned dogs with FRD were presented for clinically needed duodeno- and colonoscopy and were enrolled in a prospective placebo (PL)-controlled probiotic trial. Intestinal tissue samples and faeces were collected during endoscopy. Intestinal mRNA abundance of interleukin (IL)-5, -10, -12p40 and -13, tumour necrosis factor-alpha, transforming growth factor-beta1 and interferon (IFN)-gamma were analysed and numbers of Lactobacillus spp., Bifidobacterium spp., Enterococcus spp. and Enterobacteriaceae and supplemented probiotic bacteria were determined in faeces. The Canine Inflammatory Bowel Disease Activity Index, a scoring system comprising general attitude, appetite, faecal consistency, defecation frequency, and vomitus, decreased in all dogs (p < 0.0001). Duodenal IL-10 mRNA levels decreased (p = 0.1) and colonic IFN-gamma mRNA levels increased (p = 0.08) after probiotic treatment. Numbers of Enterobacteriaceae decreased in FRD dogs receiving probiotic cocktail (FRD(PC)) and FRD dogs fed PL (FRD(PL)) during treatment (p < 0.05), numbers of Lactobacillus spp. increased in FRD(PC after) when compared with FRD(PC before) (p < 0.1). One strain of PC was detected in five of eight FRD(PC) dogs after probiotic supplementation. In conclusion, all dogs clinically improved after treatment, but cytokine patterns were not associated with the clinical features irrespective of the dietary supplementation.