APPROACHES TO DIETARY THERAPY IN INFLAMMATORY BOWEL DISEASE

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1 Vet Times The website for the veterinary profession APPROACHES TO DIETARY THERAPY IN INFLAMMATORY BOWEL DISEASE Author : James Harris Categories : Vets Date : July 23, 2012 James Harris looks at dietary treatment and management of this condition in cats and dogs considering food types and the benefits of microorganisms Summary Inflammatory bowel disease (IBD) is a commonly diagnosed, but still relatively poorly understood, group of idiopathic conditions diagnosed in both small animals and people. This article discusses the clinician s approach to the dietary management of IBD based on an understanding of aetiology and the relative components of the diets available. Probiotics and prebiotics are also considered as adjunctive therapy and the limited scientific research is discussed. Key words inflammatory bowel disease, dietary management, probiotics and prebiotics INFLAMMATORY bowel disease (IBD) describes a group of chronic gastrointestinal (GI) disorders in dogs and cats, characterised by inflammation and mucosal cellular infiltration of the stomach, small or large intestine. Although it is frequently considered to be the commonest cause of chronic GI disease in dogs and cats, its true prevalence is unknown, which may be due, in part, to the difficulty in making a definitive diagnosis (Hall, 2012). 1 / 6

2 Inflammation may be lymphoplasmocytic, eosinophilic, neutrophilic, histiocytic or granulomatous, and may vary in location and in both histological and clinical severity. In view of this variation it is not surprising a thorough and methodical approach to diagnosis must be taken and that no single effective treatment is available for all cases. In general practice, a definitive diagnosis of IBD requires biopsy samples, often taken endoscopically ( Figure 1 ). However, there is some difficulty in assessing severity on the basis of histology alone, despite efforts by the WSAVA GI standardisation group. The interpretation can be affected by numerous factors and, hence, standardised clinical scoring systems are perhaps more reliable for example, the canine inflammatory bowel disease activity index (CIBDAI; Jergens, 2003) and the feline IBDAI (Jergens, 2010). True IBD is considered an idiopathic condition with diagnosis requiring exclusion of known causes of GI inflammation for example, endoparasites and dietary allergy (Simpson, 1996). However, more recently it has been suggested antibiotic-responsive diarrhoea, dietary allergies and steroidresponsive chronic enteropathies may all be part of a single spectrum of disease (Hall, 2012). Granulomatous colitis of young boxers and French bulldogs once considered idiopathic is now known to be caused by a specific Escherichia coli, similar to the ileum of people with Crohn s disease, and can be treated with enrofloxacin (Mansfield, 2009). Further research is ongoing into understanding the aetiology of IBD with interaction of the GI environment, diet, intestinal microflora (particularly Enterobacteriaceae) and the host immune response. Treatment of IBD Unfortunately, good quality evidence-based veterinary medicine is lacking in the effi cacy of IBD treatments and treatment decisions are based on clinical experience. The aim of treatment is to resolve the clinical signs by reducing the antigenic source of inflammation suppressing the inflammatory response while meeting the pet s nutritional requirements. Treatment often involves a combination of therapies, including dietary management, antibiotics and immunosuppressive medication. Where patients are clinically stable and not suffering from severe disease and sequelae for example, protein-losing enteropathy, dietary modification should be performed first, followed by antibiotics ( Table 1 ). Immunosuppressive drugs, such as prednisolone, should only be used when other treatments have been ineffective to differentiate idiopathic IBD from food-responsive and antibioticresponsive disease. Dietary management Dietary management is the cornerstone of IBD treatment, although unlike in adverse reactions to food ( Figure 2 ), it is unlikely to be monotherapy. However, if one considers food allergies to be on the 2 / 6

3 same spectrum of disease as IBD then the distinction is incomplete. Choice of diet for the patient should be based on the clinician s understanding of the aetiology of IBD, particularly with respect to the presence of antigenic load from bacteria and food components. The nutritional components of the diet need assessing. The diet may be home-produced, which allows better tracing of ingredients and avoidance of additives although, typically, these diets are not sufficiently well balanced for long-term use, are more expensive and time consuming. Hence, most clients will choose proprietary products, of which a large number are available. Antigenicity An elimination diet will be used in the diagnostic approach to the IBD patient. Traditionally, these have been based on the use of a novel protein and carbohydrate relying on a thorough dietary history. Food trials for GI cases can be shorter than those for dermatology, with a consensus of three to four weeks and an anticipated improvement within one to two weeks. More recently, hydrolysed diets with a single carbohydrate source have become increasingly popular. In these diets the protein is enzymatically altered, reducing its size and increasing its digestibility. The combination of the small size and novel nature of the protein reduces antigenic stimulus in the gastrointestinal tract (GIT; Biourge, 2004) and these diets can be very effective in chronic enteropathies in both cats (Mandigers, 2010) and dogs (Mandigers, 2004). Digestibility In both small and large bowel IBD, the diet digestibility is as important as antigenicity. A more digestible diet has fewer undigested protein and carbohydrate sources passing through the intestine, which both reduces the antigenic load and the substrate for bacterial growth and fermentation in the colon. The nutrients are also more easily assimilated, which is of real benefit in a typical IBD patient with malabsorption and maldigestion. Fat content The fat content of the diet is also important and the use of ubiquitous low fat diets in GI disease is now being questioned. High fat diets have traditionally been avoided as they reduce gastric transit time, stimulate nausea, and, when fatty acids are hydroxylated in the GIT by bacteria, can induce a secretory diarrhoea. However, most IBD patients can tolerate a moderate fat diet, with the exception of dogs with secondary lymphangiectasia, which requires a low fat diet. In an underweight dog with poor body condition it is acceptable to gradually increase the energy density of the diet by increasing fat levels, as long as clinical deterioration is not observed (German and Zentek, 2008). 3 / 6

4 Carbohydrate Mucosal atrophy can lead to carbohydrate malabsorption, exacerbated by bacterial overgrowth, which can cause osmotic diarrhoea. The carbohydrate source should be as digestible as possible and so rice is frequently chosen. Rice is very highly digestible, has a very low fibre content and is rarely implicated in adverse food reactions. It also improves the digestibilty of dry diets and contains soluble factors that inhibit secretory diarrhoea. Fibre High fibre diets, containing both soluble and insoluble fibre, are less digestible, but may be useful in large bowel diarrhoea as they increase faecal consistency, bind potential colonic irritants, increase colonic motility and act as prebiotics producing beneficial short-chain fatty acids. Other dietary additives may be beneficial. Increased amounts of fish oils may modulate the immune response by increasing the amount of omega 3 fatty acids in cell membranes. Antioxidants for example, vitamins C and E, iron and zinc have been shown to have protective effects in mice. Ginger is also under study, due to its antiinflammatory and antiemetic effects. Mannan oligosaccharides (MOS) are yeast wall extracts that competitively inhibit binding sites on the intestinal mucosa, reducing attachment of pathogenic bacteria. They may also stimulate local intestinal immunity by increasing the level of IgA. Sacrificial protein Theoretically, food allergy may develop secondary to IBD, due to hyperpermeability, allowing increased antigenic presentation to the gut-associated lymphoid tissue. However, this has not been proven clinically and the concept of providing a sacrificial protein has fallen out of favour. Probiotics and prebiotics Probiotics are live microorganisms that, when administered in adequate amounts, confer a health benefit on the host (Nomoto, 2005; Figure 3 ). Ideally, they should originate in the species being treated and should be non-pathogenic, resistant to digestion by gastric acid and intestinal enzymes, able to adhere to the intestinal epithelium and capable of influencing host immune responses (Wynn, 2009). Prebiotics are short or longchain oligosaccharides that are not digested and are fermented in the colon by microorganisms. They can produce short-chain fatty acids, such as butyrate, which is the preferred energy source for colonocytes among other effects. Prebiotics are generally considered to increase the number of beneficial bacteria, although there are many other rate-limiting nutrients, such as iron. 4 / 6

5 Dietary composition strongly influences the growth and replication of bacterial populations in the GIT. High protein and fat diets support bacteria, such as bacteroides and clostridia, whereas carbohydrate-rich diets support lactobacilli, bifidobacteria and eubacteria. In human medicine, research has focused on the disruption in the balance of the GI microbiome and intestinal immunity as a potential trigger for IBD. Intestinal bacteria are implicated in both human studies and experimental animal models in the pathogenesis of these disorders, although the relationship between bacteria and inflammation is more complicated than simple cause and effect (Shanahan, 2000). Unsurprisingly, there has been growing interest in using probiotics in people as an adjunct to standard anti-inflammatory medication. Good evidence exists in the human field to recommend probiotics for maintenance of remission in pouchitis, and possibly, ulcerative colitis, but not as yet for use in Crohn s disease (Veerappan et al, 2012). In dogs and cats, similar data is lacking. However, probiotics have been shown to significantly decrease the numbers of Enterobacteriaceae in dogs and may affect the balance of intestinal regulatory and pro-inflammatory cytokines (Sauter, 2006). A small prospective observational study performed on the use of a probiotic/prebiotic product in 28 dogs with undiagnosed chronic enteropathies (Pro Kolin Enterogenic, Protexin) demonstrated improvement in faecal consistency, defaecation frequency, vomiting and CIBDAI score. Probiotics hold promise in the treatment of IBD in both people and companion animals, but further work is needed to identify which probiotics are effective and in which forms of IBD. Conclusion The future of treating and managing IBD in veterinary species must be based on a better understanding of the underlying complex aetiologies of these variable idiopathic conditions. However, it is hoped that as our understanding grows, specialised diets will become increasingly productive, providing effective treatment options for even the more severe forms of the disease, with fewer side effects when compared to the current pharmacological approach. Please note some drugs mentioned in this article are used under the cascade. References Biourge V C, Fontaine J, Vroom M (2004). Diagnosis of adverse reactions to food in dogs: Efficacy of soy-isolate hydrolyzate-based diet, The Journal of Nutrition 134: 2,062-2,064. German A and Zentek J (2008). The most common digestive disease: the role of nutrition, Encyclopedia of Canine Clinical Nutrition, Royal Canin. Hall E (2012). Inflammatory bowel disease what s new? Companion 4: / 6

6 Powered by TCPDF ( Harvey R and Hall E (2009). Dietary allergy/ intolerance, Veterinary Focus 19: Jergens A E, Crandell J et al (2010). A clinical index for disease activity in cats with chronic enteropathy, Journal of Veterinary Internal Medicine 24: 1,027-1,033. Jergens A E, Schreiner C A et al (2003). A scoring index for disease activity in canine inflammatory bowel disease, Journal of Veterinary Internal Medicine 17: Mandigers P J and Biourge V (2004). Efficacy of a soy hydrolysate-based diet in the management of chronic canine gastroenteritis: A controlled study, Proceedings of the eighth meeting of the ESCVN, Budapest, Hungary: Mandigers P J, Biourge V et al (2010). A randomized open-label positively-controlled field trial of a hydrolyzed protein diet in dogs with chronic small bowel enteropathy, Journal of Veterinary Internal Medicine 24: 1,350-1,357. Mansfield C S, Jome F E, Simpson K et al (2009). Remission of hisitiocytic ulcerative colitis in boxer dogs correlates with eradication of invasive intramucosal Escherichia coli, Journal of Veterinary Internal Medicine 23: Nomoto K (2005). Prevention of infections by probiotics, Journal of Bioscience and Bioengineering 100: Sauter S N et al (2006). Effects of probiotic bacteria in dogs with food responsive diarrhoea treated with an elimination diet, Journal of Animal Physiology and Animal Nutrition (Berlin) 90: Shanahan F (2000). Probiotics and inflammatory bowel disease: is there a scientific rationale? Inflammatory Bowel Disease 6: Simpson K (1996). Small intestinal disease. In BSAVA Manual Canine and Feline Gastroenterology: Veerappan G, Betteridge J and Young P (2012). Probiotics for the treatment of inflammatory bowel disease, Current Gastroenterology Reports (epub). Wynn S (2009). Probiotics in veterinary practice, Journal of the American Veterinary Medicine Association 234: / 6

Bacteriology. Mycology. Patient: SAMPLE PATIENT DOB: Sex: MRN: Rare. Rare. Positive. Brown. Negative *NG. Negative

Bacteriology. Mycology. Patient: SAMPLE PATIENT DOB: Sex: MRN: Rare. Rare. Positive. Brown. Negative *NG. Negative Patient: SAMPLE PATIENT DOB: Sex: MRN: 3.2 0.9-26.8 U/g 1.2 0.2-3.3 mg/g 2.2 1.3-8.6 micromol/g 1.1 1.3-23.7 mg/g 1.1 0.2-3.5 mg/g Rare 1.0 0.2-8.8 mg/g Rare 4.4 2.6-32.4 mg/g 64.6 >= 13.6 micromol/g Bacteriology