Today's Veterinary Practice provides comprehensive information to keep every small animal practitioner up to date on companion animal medicine and surgery as well as practice building and management.
Issue link: http://todaysveterinarypractice.epubxp.com/i/919967
PEER REVIEWED 32 CE: INFLAMMATORY BOWEL DISEASE The focus of inflammation can exacerbate the degradation of tight junctions. T helper 1 cells and complementary T cell subsets are involved in the secretion of proinflammatory cytokines, whereas T regulatory cells antagonize proinflammatory states for appropriate homeostasis of the gut adaptive immune system. In IBD, this balance is lost. 29 Intensive and hyperresponsive states of inflammation result from aggressive T-cell responses to antigens and pathogens with upregulation of inflammatory mediators, as well as defects in microbial extermination and downregulation of inflammatory control mediators. 13,23 Environmental Factors Environmental factors encompass a number of possible etiologies. In humans with chronic enteropathies, etiologies include stress, diet, and previous exposure to pharmaceuticals, including antibiotics. 9,29,30 Although stress has not been well established in the literature as an etiology in dogs and cats, stressful events for cats have been associated with other inflammatory diseases, such as feline idiopathic cystitis and recrudescence of feline upper respiratory tract infections. 31 There is a diet-responsive component to IBD, as noted in humans. 8,12,23,29 Some cats and dogs respond favorably to novel protein and/or hydrolyzed protein diets. Because multiple dietary components are recognized by the GI immune system as foreign antigens, 32 the thought is that decreasing the load of antigens decreases inappropriate immune responses. Microbial Factors Dysbiosis, or alteration of the normal microbial ecosystem within the intestine, is also observed in IBD. 1 This has been demonstrated via fluorescence in situ hybridization analysis ( FIGURE 1 ). Reported common changes in the normal commensals include decreases in Firmicutes (eg, clostridia, bacilli), decreases in Bacteroidetes, reduced Clostridium diversity, and increases in Enterobacteriaceae (such as E coli and Pseudomonas strains). 2 Although dysbiosis would explain the occasional response to antibiotics, a number of these organisms are also found in healthy dogs and cats. Therefore, the combined action of the microbiome ecosystem and environmental factors, not solely the presence of these microflora, likely determines progression to IBD. Alteration of the microbiota by manipulation of commensals, and restricting the diet to one containing fewer structural carbohydrates and more fat, results in decreased production of short- chained fatty acids needed for overall gut health, providing further evidence for the interplay between the factors predisposing to IBD. 2,8,23 CLINICAL SIGNS Clinical signs of IBD can include vomiting, diarrhea, melena, hematochezia, weight loss, and hyporexia to anorexia, in any combination. Some patients also present with clinical signs of disease progression, such as subcutaneous edema, pleural effusion, and ascites associated with hypoalbuminemia due to a related PLE. 33 The presence of ongoing clinical signs lasting more than 3 weeks is the basis of classification of a chronic enteropathy. 34 It is important to get a full history, which includes: ■ Characterization of clinical signs ■ Duration ■ Diet ■ Therapies ■ Response to therapy This comprehensive medical history ensures proper consideration of differentials with similar presentation and an appropriate diagnostic plan. FIGURE 1. Three-color fluorescence in situ hybridization identifies Cy-3-labeled Clostridia species (labeled orange) localized within adherent mucus of a colonic biopsy specimen obtained from a dog with IBD. The mucus is also occupied by other bacteria (total bacteria labeled green with FITC-Eub). The dark blue structures are nuclei (note some epithelial cells sloughed into the mucus) stained with DAPI. Courtesy of Angela Bryan.