Interest in the composition of the intestinal microbiota and possibilities of its therapeutic modifications has soared over the last decade and more detailed knowledge specific to the canine microbiota at different mucosal sites including the gut is available. Probiotics, prebiotics or their combination (synbiotics) are a way of modifying the intestinal microbiota and exert effects on the host immune response. Probiotics are proposed to exert their beneficial effects through various pathways, for example production of antimicrobial peptides, enhancing growth of favourable endogenous microorganisms, competition for epithelial colonisation sites and immune‐modulatory functions. Despite widespread use of pro‐, pre‐ and synbiotics, scientific evidence of their beneficial effects in different conditions of the dog is scarce. Specific effects of different strains, their combination or their potential side‐effects have not been evaluated sufficiently. In some instances, in vitro results have been promising, but could not be transferred consistently into in vivo situations. Specific canine gastrointestinal (GI) diseases or conditions where probiotics would be beneficial, their most appropriate dosage and application have not been assessed extensively. This review summarises the current knowledge of the intestinal microbiome composition in the dog and evaluates the evidence for probiotic use in canine GI diseases to date. It wishes to provide veterinarians with evidence‐based information on when and why these products could be useful in preventing or treating canine GI conditions. It also outlines knowledge about safety and approval of commercial probiotic products, and the potential use of faecal microbial transplantation, as they are related to the topic of probiotic usage.

Abstract. Different antibody-based tests for rapid detection of Canine parvovirus antigens in feces are commercially available, allowing quick diagnosis in a clinical setting. However, the diagnostic accuracy of these tests compared with standard methods has not been evaluated so far. In the current study, 3 commercial tests were compared with immune-electron microscopy (IEM) and polymerase chain reaction (PCR). Dogs were divided into 3 groups: group A, samples from dogs with acute hemorrhagic diarrhea (n 5 50); group B, dogs with chronic diarrhea (n 5 10); and group C, dogs with no evidence of gastrointestinal disease (n 5 40). Specificity of all 3 commercial tests versus PCR and IEM was good to excellent (92.2-100%). Sensitivity, in contrast, was poor: 15.8-26.3% versus PCR and 50-60% versus IEM. In group A, 10 dogs were positive by IEM and 24 dogs were positive by PCR. Positive PCR results were also obtained from animals in control groups (group B, 1 dog; group C, 5 dogs). No dog in group B or C was positive by IEM. In conclusion, the rapid tests are useful to diagnose canine parvoviral enteritis, but they do not rule out parvovirus infection in an animal with typical clinical signs. In addition, a small percentage of healthy dogs and dogs with chronic diarrhea showed positive PCR results; this may be due to asymptomatic/persistent infection or intestinal passage of virus. The significance of this finding remains unclear.

Inflammasomes coordinate the maturation of IL-1β and IL-18 in response to danger signals. They are vital for maintenance of intestinal homeostasis and have been linked to chronic intestinal inflammation in humans. Probiotics have been advocated as treatment in intestinal inflammation. So far, no study has investigated the role of the inflammasome in canine chronic enteropathy (CE). In this study the intestinal expression of inflammasome components was assessed in CE dogs compared to controls, when treated with probiotic Enterococcus faecium (EF) ex-vivo and in-vivo. RNA extraction from endoscopic biopsies and reverse-transcriptase quantitative PCR was performed for NLRP3, casp-1, IL-1β and IL-18. Immunohistochemistry was performed to investigate protein expression in tissues. Gene expression of casp-1 and NLRP3 was lower in CE samples than controls. Ex-vivo treatment with EF reduced NLRP3 expression in control samples. Treatment of CE dogs with EF alongside dietary intervention had no effect on gene expression. In contrast, IL-1β protein expression in CE decreased with dietary treatment (but not with probiotics). The results of this study suggest that the inflammasome or its components may be partially involved in the inflammatory process seen in CE, but distinct from intestinal inflammation in humans.

BackgroundCanine chronic enteropathies (CE) are believed to be caused by an aberrant immune response towards the intestinal microbiome. Administration of probiotics can alleviate colitis in people. In vitro effects of the probiotic Enterococcus faecium NCIMB 10415 E1707 (EF) previously have been evaluated using canine cells (e.g., whole blood, intestinal biopsies), but data on in vivo efficacy are lacking.Hypothesis/ObjectivesAdministration of EF to dogs with food‐responsive CE will improve clinical outcome and decrease the intestinal inflammatory profile.AnimalsDogs diagnosed with CE were prospectively recruited to receive a hydrolyzed elimination diet plus either a synbiotic product containing EF or placebo for 6 weeks. Both veterinary staff and owners were blinded to the treatment.MethodsClinical severity index (CCECAI), clinicopathological data and gene expression using intestinal biopsies (TLR2/4/5/9, IL‐17A, IL‐22, IL‐23p19, RORC, IL‐2, IL‐12p35, TNFα, IL‐4, IFNy, IL‐10, TGFβ, IL‐1β, IL‐18, NLRP3, casp‐1, TFF1, TFF3 and PPARy) before and after 6 weeks of treatment were analyzed using linear mixed modeling.ResultsOf the 45 cases recruited, 12 finished the clinical trial. Seven received the synbiotic and 5 the placebo product. There was no difference between groups or treatments regarding clinical efficacy, histology scores or expression of any of the investigated genes.Conclusions and clinical importanceStandard dietary treatment induced rapid clinical response in all cases. Because the study was underpowered, it was not possible to determine whether or not EF had an additional effect within the time period of 6 weeks.