Effects of Canine-Obtained Lactic-Acid Bacteria on the Fecal Microbiota and Inflammatory Markers in Dogs Receiving Non-Steroidal Anti-Inflammatory Treatment.

Non-steroidal anti-inflammatory drugs (NSAIDs) may cause enteropathy in dogs and probiotics may be one option to prevent this. The objective of this study was to determine whether the administration of canine-obtained lactic acid bacteria (LAB) has an effect on the frequency of diarrhea, the composition of the fecal microbiota, and/or markers of gastrointestinal inflammation in dogs receiving NSAIDs when compared to dogs given NSAIDs and a placebo. A total of 22 dogs treated with NSAIDs for various clinical indications were enrolled in a seven-day randomized, double-blinded placebo-controlled interventional study. Dogs were randomized to receive either placebo or LAB, a product containing Limosilactobacillus fermentum, Lacticaseibacillus rhamnosus, and Lactiplantibacillus plantarum. Fecal samples were collected on days one and seven. The fecal microbiota was evaluated using the fecal dysbiosis index (DI) and individual bacterial taxa. Fecal calprotectin (CP) and S100A12/Calgranulin C concentrations were used as markers of gastrointestinal inflammation. There was a difference in frequency of diarrhea between groups, with it affecting 4/12 dogs (33%) in the placebo group and 1/10 dogs (10%) in the LAB group, but this difference did not reach statistical significance (p = 0.32). There was a correlation between S100A12 and CP (p < 0.001), and Clostridium perfringens correlated with S100A12 (p < 0.015). Neither treatment significantly affected S100A12 (p = 0.37), CP (p = 0.12), or fecal DI (p = 0.65). This study suggests that LAB is a safe supplement to use for short-term treatment in NSAID-treated dogs, but further studies are needed to determine its potential to prevent NSAID-induced enteropathy in dogs.

Changes in the fecal microbiota in dogs with acute hemorrhagic diarrhea during an outbreak in Norway.

BACKGROUND: A severe form of acute hemorrhagic diarrhea syndrome (AHDS) occurred in dogs in the Oslo region of Norway during autumn 2019. OBJECTIVES: To characterize the fecal microbiota of dogs with AHDS during the outbreak and compare it to that of healthy dogs from the same period and before the outbreak. ANIMALS: Dogs with AHDS (n = 50), dogs with nonhemorrhagic diarrhea (n = 3), and healthy dogs (n = 11) were sampled during the outbreak. In addition, 78 healthy dogs from the same region were sampled before the outbreak between 2017 and 2018. METHODS: Retrospective case-control study. The fecal microbiotas were characterized using 16S rRNA gene amplicon sequencing. RESULTS: Dogs with AHDS had significantly different microbiota composition (R2  = .07, P < .001) and decreased intestinal diversity relative to healthy dogs from the outbreak period (median, 2.7; range, 0.9-3.5 vs median, 3.2; range, 2.6-4.0; P < .001). The microbiota in dogs with AHDS was characterized by a decrease of Firmicutes and an outgrowth of Proteobacteria, with increased numbers of Clostridium perfringens and Providencia spp. Among the Providencia spp., 1 showed 100% sequence identity with a Providencia alcalifaciens strain that was cultivated and isolated from the same outbreak. No Providencia spp. was found in healthy dogs sampled before the outbreak. CONCLUSIONS AND CLINICAL IMPORTANCE: Dogs with AHDS had marked changes in fecal microbiota including increased numbers of Providencia spp. and C. perfringens, which may have contributed to the severity of this illness.

Immunohistochemical expression of ß-catenin, Ki67, CD3 and CD18 in canine colorectal adenomas and adenocarcinomas.

BACKGROUND: Inflammation is believed to influence human colorectal carcinogenesis and may have an impact on prognosis and survival. The mucosal immunophenotype in dogs with colorectal cancer is poorly described. The aim of this study was to investigate whether the density, distribution and grade of tumor-infiltrating immune cells (TIIs) are different in normal colonic tissue vs benign stages (adenomas) and malignant stages (adenocarcinomas) of canine colorectal carcinogenesis, and thus, whether they can be considered as prognostic factors in dogs. This retrospective case-control study was performed on formalin-fixed, paraffin-embedded tissue samples from dogs with histologically confirmed colorectal adenoma (n = 18) and adenocarcinoma (n = 13) collected from archived samples. The samples had been collected by colonoscopy, surgery or during postmortem examination. Healthy colonic tissue obtained post mortem from dogs euthanized for reasons not involving the gastrointestinal tract served as control tissue (n = 9). RESULTS: The tumor samples had significantly lower numbers of CD3+ T-cells in the epithelium compared to controls (adenocarcinoma vs control, Kruskal-Wallis test, p = 0.0004, and adenoma vs control, p = 0.002). Adenomas had a significantly lower number of CD18+ cells in the lamina propria, compared to control samples (Kruskal-Wallis test, p = 0.008). Colonic samples from control dogs had uniform staining of ß-catenin along the cell membrane of epithelial cells. Compared to normal colonic cells, the expression levels of cytoplasmic ß-catenin were significantly higher in adenomas and adenocarcinomas (adenoma vs control Kruskal-Wallis test, p = 0.004, and adenocarcinoma vs control, p = 0.002). None of the control samples showed positive staining of ß-catenin in the nucleus of colonic cells. In contrast, adenocarcinomas and adenomas showed moderate to strong staining of the cell nucleus. The nuclear ß-catenin expression (signal strength and distribution) was significantly higher in adenomas compared to adenocarcinomas (Kruskal-Wallis test, p < 0.05). CONCLUSIONS: ß-catenin and Ki67 were not useful markers for demonstrating tumor progression from adenomas to adenocarcinomas. The lower presence of CD18 and CD3+ cells in colorectal tumors compared to controls indicates a reduced presence of histiocytes and T-cells, which may have implications for the pathogenesis and progression of colorectal cancer in dogs.

A diet change from dry food to beef induces reversible changes on the faecal microbiota in healthy, adult client-owned dogs.

BACKGROUND: Diet has a major influence on the composition of the gut microbiota, whose importance for gut health and overall well-being is increasingly recognized. Knowledge is limited regarding health implications, including effects on the faecal microbiota, of feeding a diet with high content of red meat to dogs, despite some owners' apparent preference to do so. The aim of this study was to evaluate how a diet change from commercial dry food to one with a high content of boiled minced beef and vice versa influenced the faecal microbiota, and short chain fatty acid profile in healthy, adult, client-owned dogs. RESULTS: The diet change influenced the faecal microbiota composition and diversity (Shannon diversity index). The most abundant OTUs in samples of dogs fed the dry food and high minced beef were affiliated with the species Faecalibacterium prausnitzii and Clostridia hiranonis respectively. The high minced beef diet apparently also influenced the short chain fatty acid profile, with increased isovaleric acid, as well as an increase in faecal pH. These effects were reversed when the commercial dry food was reintroduced in weeks 6 and 7. CONCLUSIONS: Results of this study can aid in the understanding of how diet changes influence the faecal microbiota and metabolite content on a short-term basis. Long-term studies are required to investigate potential implications for canine gut and general health.