Inflammatory bowel disease (IBD) has been an important topic of discussion and research in canine and feline gastroenterology for more than 20 years.
Inflammatory bowel disease (IBD) has been an important topic of discussion and research in canine and feline gastroenterology for more than 20 years. At times, IBD has been stated to be the most common cause of chronic gastrointestinal signs in dogs and cats. Small intestinal IBD can be particularly devastating, as severe weight loss with or without hypoalbuminemia may occur (Figure 1).
Figure 1. A dog with severe weight loss caused by small intestinal disease.
One of the problems with IBD is that different definitions have been applied, and there has been no clear consensus as to exactly what constitutes IBD. In some cases, IBD has been referred to in the context of a histologic diagnosis, diagnosed solely by finding inflammation in intestinal biopsies (Figures 2 & 3); while in other cases, IBD has been defined as idiopathic intestinal inflammation, in which histology by itself is inadequate for diagnosis. Our current collective term for canine and feline IBD describes persistent or recurrent gastrointestinal signs that have histologic evidence of inflammatory infiltration of the small or large intestinal mucosa of unknown cause. Current thought is that the condition can only be called IBD if no underlying cause for the inflammation can be found.1
Figure 2. A duodenal biopsy section from a 3-year-old Yorkshire terrier with IBD showing increased numbers of lymphocytes and plasma cells in the lamina propria (hematoxylin-eosin stain; bar = 50 μm). Courtesy of Dr. Penny Watson, Cambridge University Veterinary School.
Recently, new evidence suggests that intestinal bacteria probably play an important role in the initiation or perpetuation of the intestinal inflammation that has been termed IBD.1-5 Unfortunately, histology by itself cannot distinguish idiopathic intestinal inflammation from intestinal inflammation due to these gut bacteria or diet.
Figure 3. The endoscopic appearance of the duodenal mucosa in a dog with severe mucosal inflammation. In this case, no cause could be found, and the diagnosis became IBD.
With the advantage of hindsight, we can now see that the effectiveness of metronidazole in treating IBD should have been an early clue to the potential importance of bacteria as a cause of IBD. Metronidazole has benefitted many patients diagnosed as having IBD because of what was hypothesized to be an immunomodulatory effect.6 However, current thought is that metronidazole may be beneficial in these patients because of its efficacy in killing anaerobic bacteria. Another clue has been the finding that many dogs and some cats with steroid-resistant IBD may respond better to an elimination diet trial or antimicrobial therapy than to anti-inflammatory drugs.
While much of this evidence is anecdotal, there are published accounts of antibiotics (e.g. tylosin) "curing" what was diagnosed as IBD dating back 30 years.7 Since then, the efficacy of tylosin has been confirmed in other studies,8 which has helped reveal the potential role that bacteria play in causing or maintaining the intestinal inflammation in patients with IBD.1-5 Recently, the term dysbiosis has been suggested as a better description of what is occurring in the intestines of patients with IBD.
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Dysbiosis refers to an imbalance in the commensal intestinal bacterial population such that bacterial species that tend to favor inflammation in the intestinal mucosa (e.g. Escherichia coli) are overrepresented while those species that are less likely to induce inflammation (e.g. Bifidobacterium species) are underrepresented. The result is initiation and/or perpetuation of intestinal inflammation.
While antibiotics (e.g. tylosin) have been effective in treating untold numbers of dogs and cats with chronic gastrointestinal disease that were rightly or wrongly diagnosed as having IBD, there are important potential downsides to the use of antibiotics. In particular, there is growing concern over the development of antibiotic resistance associated with long-term use of antibiotics in animals. While this article is not the forum to discuss whether antibiotic resistance is the fault of veterinarians or physicians, one point that is not in dispute is that responsible use of antibiotics is an ethical imperative. Therefore, it is reasonable to explore other methods of altering or modulating intestinal bacterial ecosystems or their effect upon the intestinal tract. Prebiotics and probiotics are two possibilities that bear investigation.
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Prebiotics are dietary fibers (e.g. fructooligosaccharides or xylooligosaccharides) that cannot be metabolized by mammals but that preferentially feed some bacterial species ("good" bacteria that benefit the patient), theoretically giving these species a competitive advantage over less desirable bacteria that may harm the patient.
In one study, prebiotics were beneficial in treating dogs with suspected small intestinal bacterial overgrowth, or SIBO (see the Related Link "Prebiotics Research").9 Of course, one report— particularly an abstract—is not proof of efficacy, and so additional studies confirming this study's findings are needed before sweeping statements can be made. But studies such as this one are reasonable justification to continue looking at the modulation of intestinal bacteria populations with carefully designed clinical trials using prebiotics or probiotics.
Educating clients about IBD
Michael Willard, DVM, MS, DACVIM
Department of Small Animal Clinical Sciences
College of Veterinary Medicine
Texas A&M University
1. Washabau RJ, Day MJ, et al. Endoscopic, biopsy, and histopathologic guidelines for the evaluation of gastrointestinal inflammation in companion animals. The WSAVA International Gastrointestinal Standardization Group, 2009 ACVIM Consensus Statement. J Vet Intern Med 2010;24(l): 10-26.
2. Simpson KW. Host floral interactions in the gastrointestinal tract. ACVIM Forum, Montreal, Canada 2009:437-439.
3. Xenoulis PG, Palculict B, et al. Molecular-phylogenetic characterization of microbial communities imbalances in the small intestine of dogs with inflammatory bowel disease. FEMS Microbiol Ecol 2008;66:579-589.
4. Janeczko S, Atwater D, et al. The relationship of mucosal bacteria to duodenal histopathology, cytokine mRNA, and clinical disease activity in cats with inflammatory bowel disease. Vet Microbiol 2008;128:178-193.
5. Craven M, McDonough DS, Simpson KW. High throughput pyrosequencing reveals reduced bacterial diversity in the duodenal mucosa of dogs with IBD. J Vet Intern Med 2009;23:731 [abstract].
6. Tarns TR. Chronic ferine inflammatory bowel disorders. Part I idiopathic inflammatory bowel disease. Compend Contin Educ 1986;8:371-376.
7. van Kruiningen H. Clinical efficacy of tylosin in canine inflammatory bowel disease. J Am Arum HospAssoc 1976;12:498-501.
8. Westennarck E, Skrzypczak T, et al. Tylosin-responsive chronic diarrhea in dogs. J Vet Intern Med 2005;19:177-186.
9. Ruaux CG, Tetrick MA, Steiner JM, et al. Fecal consistency and volume in dogs with suspected small intestinal bacterial overgrowth receiving broad spectrum antibiotic therapy or dietary fructo-oligosaccharide supplementation. J Vet Intern Med 2004;18:425 [abstract].
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