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Veterinarian Technician October 2011 (Vol 32, No 10)

Inflammatory Bowel Disease in Cats

by Kathleen Dunbar, BA, RVT

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    Inflammatory bowel disease (IBD) is used to describe a group of gastrointestinal (GI) diseases commonly diagnosed in adult cats. The prevalence and cause of IBD are unknown. Idiopathic by definition, IBD is characterized by inflammation of the stomach, small intestine, and/or large intestine with associated GI signs, including vomiting or diarrhea lasting more than 3 weeks. IBD is not remedied by food trials or definitively ruled out using most diagnostics. IBD can be confirmed only by biopsy.

    Key Points

    • IBD is diagnosed by ruling out other causes of GI distress and is confirmed by biopsy.
    • IBD is thought to result from dysfunctional interplay between the mucosal barrier, mucosal immunity, and microflora.
    • Treatment of IBD may involve dietary change and/or medication. Strict owner compliance is required, and recurrence is possible.

    Types of Inflammatory Bowel Disease

    The types of IBD are classified by the principal inflammatory cells infiltrating the GI tract.1 Most of these cell lines can be found in cases of IBD, but certain ones are more common. Lymphocytic-plasmacytic IBD, which infiltrates the lamina propria, is most common. Eosinophilic IBD and suppurative IBD are less common, typically invading one of two layers of the intestinal tract. Neutrophilic IBD and granulomatous IBD are rare.


    Adaptive immune system—composed of specialized lymphocytes, this system recognizes pathogens it has previously encountered, providing immunity to anticipated pathogens

    Innate immune system—a body’s first line of defense, this system does not have specialized cells and, therefore, does not provide long-term immunity to challenges

    Nucleotide-binding oligomerization domain containing 2 (NOD2) receptor—a type of pattern-recognition receptor, NOD2 proteins work intracellularly to activate an immune response; NOD2 receptors specifically recognize muramyl dipeptide, which is found in certain strains of bacteria

    Pattern-recognition receptor (PRR)—proteins that recognizemolecules unique to a specific microorganism

    Toll-like receptor (TLR)—a type of PRR, TLRs play a critical role in the body’s immune system response; they recognize microbes that have invaded the intestinal tract mucosa and stimulate a response from the immune system


    No studies have confirmed the etiology of IBD in cats. Therefore, information on the cause of IBD has been based on human and murine studies. Although significant clinical and histologic differences exist between cats and humans, the pathogenesis of IBD is thought to be similar in both species.1

    Box 2. Abnormal Mucosal Microflora7–9

    In one study, mucosal Enterobacteriaceae spp accounted for 66% of total bacteria in cats with IBD, but 0.3% in healthy cats. In another study involving mice, germ-free control subjects did not develop IBD, whereas mice with normal bacterial flora developed the disease.

    The development of IBD is hypothesized to be due to interplay between (1) a disturbance in the GI mucosal barrier, (2) mucosal immunity, and (3) mucosal microflora.2 In a normal GI tract, a healthy epithelial lining protects the mucosal barrier with innate and adaptive immune responses to insults. Receptors on and within epithelial cells control the innate and adaptive immune responses and affect the interplay between the mucosal barrier, immunity, and microflora3–5 ( BOX 1 2–6). Malfunctioning receptors disrupt homeostasis.1,6 Abnormal numbers of mucosal microflora may also be involved in the pathogenesis of IBD7 (BOX 27–9). Bacterial populations that are likely to induce inflammation increase in number, and commensal bacteria decrease in number. Large numbers of mucosal bacteria are associated with a faulty mucosal barrier, a cytokine mRNA response, and increased clinical signs.8 The interactions between the defective mucosal barrier, immunity, and microflora encourage chronic inflammation and clinical signs.

    Clinical Findings

    Clinical signs of IBD can vary significantly among patients, depending on the anatomic location of the associated inflammation.1,10 Signs can appear and disappear sporadically. Vomiting and diarrhea are the most common signs. If the small intestine is inflamed, abdominal discomfort may be detected on palpation. Cats with inflammation of the large intestine may be painful on rectal palpation. In severe cases, the following can be present: weight loss, appetite changes, poor haircoat, mucoid feces, tenesmus, increased frequency of defecation, and hematochezia.

    Male and female cats share the same disease predisposition.11 The mean age for development is 5.2 years.11 Siamese and exotic breeds appear to be at increased risk of developing lymphocytic-plasmacytic IBD, but no definitive breed predilection has been reported.11 The pancreatic and biliary ducts are combined in cats, so IBD, lymphocytic cholangitis, and chronic pancreatitis can be associated with each other.12,13 Other than the cited breed associations, genetic influences have not been identified in cats; however, a gene mutation identified in humans may be applicable to cats.14


    Box 3. Ruleouts for IBD

    • Endocrinopathies (e.g., hyperthyroidism, diabetes mellitus)
    • FeLV, FIV, coronavirus
    • Renal disease
    • Helminth infection, giardiasis, salmonellosis, campylobacteriosis, Tritrichomonas foetus infection, Clostridium spp infection)
    • Food allergy or intolerance
    • Neoplastic growth
    • Systemic disease (renal or hepatic)
    • Foreign body
    • Motility disorder
    IBD is diagnosed by ruling out other causes of inflammation. The following must be investigated in a step-by-step manner, but not necessarily in the following order: infectious or parasitic pathologies, food sensitivity or intolerance, endocrine or metabolic disturbances, foreign bodies, or neoplastic diseases of the GI tract (BOX 3). Empirical treatment should be initiated for suspected conditions. After the possibility of these diseases and conditions has been eliminated, the following clinical criteria must be met to confirm a diagnosis15:

    • The cat has shown chronic GI clinical signs for at least 3 weeks

    • Other conditions (BOX 3) have been eliminated as likely causes of the inflammation

    • Food trials and antibacterial and anthelmintic treatment provide incomplete relief of clinical signs

    • The cat has responded well to antiinflammatory and/or immunosuppressant medications

    • Biopsy shows evidence of mucosal inflammation consistent with IBD

    Laboratory Findings and Diagnostic Imaging

    Laboratory findings can rule out other disorders1,10 and support a diagnosis of IBD. In IBD of the small intestine, serum biochemistry panels may show hypercholesterolemia, hypocalcemia, and hypomagnesemia. Hematology may show neutrophilia with or without a left shift. Anemia may be present because of chronic inflammation or chronic blood loss. These findings are not as common in IBD of the large intestine. The C-reactive protein level, which surges in response to inflammation, may be increased in severe IBD of the small or large intestine.16 Fecal α1-protease inhibitor activity tests can be used to detect protein-losing enteropathies before hypoproteinemia is apparent.17 Cats with IBD often have high trypsin-like immunoreactivity concentrations, which points toward simultaneous pancreatic disease. Increased hepatic values are frequently seen.

    Cats with IBD sometimes have low serum folate and cobalamin concentrations.18–20 Folate is absorbed by the proximal small intestine, and cobalamin is absorbed in the ileum. These test results are consistent with a diagnosis of IBD and may help determine the location of the inflammation.

    Radiography, including contrast studies, has limited value, except to rule out a foreign body; however, ultrasonography is an important diagnostic measure. Thickening of the large and small intestinal walls and enlarged lymph nodes are common ultrasonographic findings.21 They are characteristic of inflammatory disease processes but are not specific to IBD. Ultrasonography can provide information on the location and severity of lesions, suggesting whether a biopsy should be performed endoscopically or surgically.

    Food Trials

    To diagnose IBD, food allergies and intolerances must be ruled out. Except for very mild IBD, the disease does not respond to dietary manipulation alone. However, idiopathic GI signs resolve in up to 50% of cats placed on an elimination diet.22 Thesecats are presumed to have a food allergy or intolerance instead of IBD. At presentation, some cats are too fragile to begin a food trial and need immediate empirical treatment, which eliminates a food trial as a diagnostic possibility. If a food trial is permissible, a 4- to 6-week trial is recommended, although shorter trials have been adequate.1,10,22


    Histopathology is the only way to confirm IBD. However, histopathologic findings vary significantly among pathologists.23 Until recently, a lack of standard criteria clouded agreement on the normal histology of cats with IBD. Guidelines, including pictorial templates and standard reporting forms advocated by the World Small Animal Veterinary Association Gastrointestinal Standards Group, aim to reduce the subjectivity of histology.24 With the use of objective criteria, a sample of mucosa can be identified as normal or diseased. If diseased, a sample can show the severity of the disease, morphologic abnormalities, and predominant inflammatory cells.

    Biopsy samples are most simply obtained using endoscopy, which is less invasive, less expensive, and more appropriate for frail cats. However, endoscopy allows sampling of only the mucosal layer of the proximal GI tract. Full-thickness and extraintestinal biopsies are important diagnostic tools25–27; if they are not obtained, a diagnosis may be missed or a misdiagnosis can be made (e.g., IBD can be easily confused with lymphoma). Although surgical and laparoscopic biopsies are complex, they are preferred.

    Clients should be encouraged to allow a biopsy before any other diagnostic procedure or therapies. Obtaining a biopsy sample is sometimes difficult because of financial restrictions or poor condition of the patient. Clients should be made aware that biopsies performed after therapy has begun may not be diagnostically accurate. Furthermore, cats with undiagnosed diseases such as lymphoma may initially respond well to IBD treatment, obscuring the true diagnosis.


    Well-controlled studies examining the efficacy of IBD treatment are absent. Instead, treatment relies on clinical experience. Treatment is aimed at reducing the antigenic source of inflammation and suppressing the inflammatory response. Treatment focuses on diet, supplementation, and pharmaceutical therapies.

    Diet and Supplementation

    According to the definition of IBD, an affected cat has an incomplete response to dietary modification. However, cats with mild IBD may be food-responsive because dietary antigens play a role in its etiology.2,6 Dietary changes can play a key role in IBD therapy. Food intolerances or allergies may develop secondary to IBD, so a dietary change may be called for in these situations. In more severe IBD, dietary changes should be used in combination with other IBD therapies. Low-antigen, easily digested diets from a single protein source may decrease the antigen load on the GI tract. Cats with eosinophilic IBD may respond well to a hypoallergenic diet, while a high-fiber diet may be helpful in colonic IBD.1,10

    The therapeutic use of probiotics and prebiotics is gaining popularity. Probiotics are live microorganisms that may help protect the mucosal barrier and balance microorganisms in the intestines. Prebiotics are nondigestible materials in food that may support growth of resident gut bacteria and suppress the immune response.

    Human and canine IBD studies support the use of prebiotics and probiotics.28,29 Little research has been done on cats, but initial studies and clinical experience have shown the use of probiotics to be of value.30 The limited feline studies on the use of prebiotics have found no significant changes to bacterial flora.31 Further feline studies exploring their use may document therapeutic value.

    Cats with IBD, especially those with weight loss, often have low cobalamin levels because of intestinal malabsorption. A low cobalamin level affects GI function, contributing to clinical signs.18,19,32 Cobalamin deficiency can be treated with subcutaneous injections. If this deficiency is not corrected, an affected cat continues to show clinical signs despite pharmaceutical and dietary intervention.

    Folate deficiency in cats can result in anemia, anorexia, and lethargy.20 Folate (400 µg PO q24h for 6 weeks) should be given to compensate for decreased proximal intestinal absorption.33

    Pharmaceutical Treatment

    Although they can have adverse effects, corticosteroids are the pharmaceutical cornerstone of IBD therapy because they disrupt the inflammatory pathways of the GI tract. Prednisone, prednisolone, and methylprednisolone are recommended. Budesonide has been useful in humans and dogs with IBD, but clinical use of the drug in cats has had variable success.1,10 No studies have examined the effectiveness or long-term risk of using budesonide in cats.

    Cats with refractory clinical signs or steroid-induced morbidity require additional management. The cytotoxic drug chlorambucil is an adjunct to steroid therapy and can be given until remission occurs.1,10 Leukopenia is an uncommon adverse effect of chlorambucil, so regular blood work is important.34 The use of cyclosporine has been helpful in dogs, and anecdotal evidence supports use of this drug in cats. Latent infections such as toxoplasmosis may appear with the use of cyclosporine in cats.1,10,35

    Metronidazole is an antimicrobial that affects the innate and adaptive GI immune responses. Although this drug’s mechanism of action is not completely understood, the drug is known to help balance intestinal microflora, reduce obligate anaerobe load, and reduce inflammation. The use of metronidazole benzoate is recommended because anorexia and hypersalivation have been linked to the use of metronidazole hydrochloride.36–38 Metronidazole benzoate contains 60% metronidazole, so the drug must be dosed at 25 mg/kg instead of 15 mg/kg.37 Metronidazole should not be used indefinitely because of the risk of neurotoxicosis, genotoxicosis, and liver insufficiency.36–40


    The prognosis for cats with IBD is frequently positive. Mild cases may respond to metronidazole therapy alone, and remission can extend for long periods.1,10 Cats are unlikely to immediately develop serious metabolic side effects from steroid use.1 In some cases, the prognosis is poor. A decreased cobalamin level is associated with weak response to treatment.18,19,32 C-reactive protein may be a marker of the prognosis because increased levels in humans correlate with chronic and refractory inflammation.41 Research has raised the possibility that alimentary lymphoma in cats is the result of previous IBD.1,10

    Disease markers such as C-reactive protein can be incorporated into clinical indices, which are valuable for assessing the course of a disease. Such indices exist for canine and human IBD, and a clinical index called feline chronic enteropathy activity index (FCEAI) was recently developed for cats with enteropathies13,42 (BOX 4) . The numeric scores can be used to measure the initial assessment, predict the response to treatment and the possibility of remission, and determine a prognosis. The clinical signs and severity of IBD vary significantly in cats, so numeric scores can more accurately define disease activity for clinical and research purposes.

    Client Education

    The technician’s role in educating clients about IBD is a valuable part of a cat’s recovery. The time-consuming nature of diagnosing IBD and stabilizing an affected patient makes client communication particularly important. Technicians should be able to clearly answer client questions about the diagnostic process, the disease, and the reasonable expectations. Remissions and setbacks are common with IBD, so technicians should offer support when clients are feeling uncertain about their cats’ progress.

    Clients may resist changing their pets’ diet and routine. Some researchers have speculated that cats and dogs with IBD may be unresponsive to treatment because of client noncompliance with food restrictions or with administration of medications.43 Clients may hastily stop drug treatment if adverse effects appear or if clinical signs of IBD disappear. Technicians should show clients how to properly medicate their cats, discuss potential adverse effects, and emphasize the need for long-term treatment. Technicians play an important role in supporting clients to ensure compliance with using a new food and/or medication.


    Technicians are likely to frequently see cats with IBD. By understanding the pathogenesis and management of this disease (including potential adverse effects and nonmedical supplements), technicians can support clients in a possibly lifelong commitment to managing IBD.

    Downloadable PDF

    1. Hall EJ, German AJ. Diseases of the small intestine. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis, MO: Elsevier Saunders; 2010:1526-1572.

    2. Sartor RB. Microbial and dietary factors in the pathogenesis of chronic, immune-mediated intestinal inflammation. Adv Exp Med Biol 2006;579:35-54.

    3. Abreu MT, Fukata M, Arditi M. TLR signaling in the gut in health and disease. J Immunol 2005;174(8):4453-4460.

    4. Gribar SC, Anand RJ, Sodhi CP, Hackham DJ. The role of epithelial toll-like receptor signaling in the pathogenesis of intestinal inflammation. J Leukoc Biol 2008;83(3):493-498.

    5. Cario E. Bacterial interactions with cells of the intestinal mucosa: Toll-like receptors and NOD2. Gut 2005;54(8):1182-1193.

    6. Cameiro LAM, Magalhaes JG, Tattoli I, et al. NOD-like proteins in inflammation and disease. J Pathol 2008;214(2):136.

    7. Zakharchenko MP, Zakharchenko MM, Zakharchenko VM, et al. A problem in health rehabilitation in the development of dysbioses under the influence of environmental factors. Gig Sanit 2005;6:72-75.

    8. Janeczko S, Atwater D, Bogel E, 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(1-2):178-193.

    9. Nell S, Suerbaum S, Josenhans C. The impact of the microbiota on the pathogenesis of IBD: lessons from mouse infection models. Nat Rev Microbiol 2010;8(8):564-577.

    10. Hall EJ, German AJ. Diseases of the large intestine. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis, MO: Elsevier Saunders; 2010:1573-1594.

    11. Dennis JS, Kruger JM, Mullaney TP. J Am Vet Med Assoc 1993;202(2):313-318.

    12. Weiss DJ, Gagne JM, Armstrong PJ. Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats. J Am Vet Med Assoc 1996;209(6):1114-1116.

    13. Jergens AE, Crandell JM, Evans R, et al. A clinical index for disease activity in cats with chronic enteropathy. J Vet Intern Med 2010;24(5):1027-1033.

    14. Hugot JP. Role of NOD2 gene in Crohn's disease. Gastroenterol Clin Biol 2002;26(1):13.

    15. World Small Animal Veterinary Association. WSAVA and Committee Projects: GI Standardization Group. www.wsava.org/StandardizationGroup.htm. Accessed October 2010.

    16. Ceron JJ, Eckersall PD, Martýnez-Subiela S. Acute phase proteins in dogs and cats: current knowledge and future perspectives. Vet Clin Pathol 2005;34(2):85-99.

    17. Fetz K, Steiner JM, Broussard JD, et al. Evaluation of fecal alpha1-proteinase inhibitor concentrations in cats with inflammatory bowel disease and cats with gastrointestinal neoplasia. J Vet Intern Med 2005;19(3):439.

    18. Simpson KW, Fyfe J, Cornetta A, et al. Subnormal concentrations of serum cobalamin (vitamin B12) in cats with gastrointestinal disease. J Vet Intern Med 2001;15(1):25-32.

    19. Reed N, Gunn-Moore D, Simpson K. Cobalamin, folate and inorganic phosphate abnormalities in ill cats. J Feline Med Surg 2007;9(4):278-288.

    20. Suchodolski JS, Steiner JM. Laboratory assessment of gastrointestinal function. Clin Tech Small Anim Pract 2003;18(4):203-210.

    21. Baez JL, Hendrick MJ, Walker LM, Washabau RJ. Radiographic, ultrasonographic, and endoscopic findings in cats with inflammatory bowel disease of the stomach and small intestine: 33 cases (1990-1997). J Am Vet Med Assoc1999;215(3):349-354.

    22. Guilford WG, Jones BR, Markwell PJ, et al. Food sensitivity in cats with chronic idiopathic gastrointestinal problems. J Vet Intern Med 2001;15(1):7-13.

    23. Willard MD, Jergens AE, Duncan RB, et al. Interobserver variation among histopathologic evaluations of intestinal tissues from dogs and cats. J Am Vet Med Assoc 2002;220(8):1177-1182.

    24. Washabau R, Day M, Willard M., et al. Endoscopic, biopsy, and histopathologic guidelines for the evaluation of gastrointestinal inflammation in companion animals. J Vet Intern Med 2010;24(1):10-26.

    25. Kleinschmidt S, Harder J, Nolte I, et al. Chronic inflammatory and non-inflammatory diseases of the gastrointestinal tract in cats: diagnostic advantages of full-thickness intestinal and extraintestinal biopsies. J Feline Med Surg 2010;12(2):97-103.

    26. Evans SE, Bonczynski JJ, Broussard JD, et al. Comparison of endoscopic and full-thickness biopsy for diagnosis of inflammatory bowel disease and alimentary tract lymphoma in cats. J Am Vet Med Assoc 2006;229(9):1447-1450.

    27. Zwingenberger AL, Marks SL, Baker TW, Moore PF. Ultrasonographic evaluation of the muscularis propria in cats with diffuse small intestinal lymphoma or inflammatory bowel disease. J Vet Intern Med 2010;24(2):289-292.

    28. Damaskos D, Kolios G. Probiotics and prebiotics in inflammatory bowel disease: microflora ‘on the scope.’ Br J Clin Pharmacol 2008;65(4):453-467.

    29. Biagi G, Cipollini I, Pompei A, et al. Effect of a Lactobacillus animalis strain on composition and metabolism of the intestinal microflora in adult dogs. Vet Microbiol2007;124(1-2):160-165.

    30. Marshall-Jones ZV, Baillon ML, Croft JM, Butterwick RF. Effects of Lactobacillus acidophilus DSM13241 as a probiotic in healthy adult cats. Am J Vet Res2006;67(6):1005-1012.

    31. Sparkes AH, Papasouliotis K, Sunvold G, et al. Bacterial flora in the duodenum of healthy cats, and effect of dietary supplementation with fructo-oligosaccharides. Am J Vet Res 1998;59(4):431-435.

    32. Ruaux CG, Steiner JM, Williams DA. Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. J Vet Intern Med 2005;19(2):155-160.

    33. Gaspar M.Supplementing cat with taurine and folate.Veterinary Information Network. Internal Medicine: Feline; June 2009. http://www.vin.com/Members/boards/discussionviewer.aspx?FirstMsg=1&LastMsg=20&DocumentId=3528344. Accessed August 2011.

    34. Kiselow MA, Rassnick KM, McDonough SP, et al. Outcome of cats with low-grade lymphocytic lymphoma: 41 cases (1995–2005). J Am Vet Med Assoc 2008;232(3):405-410.

    35. Barrs VR, Martin P, Beatty JA. Antemortem diagnosis and treatment of toxoplasmosis in two cats on cyclosporin therapy. Aust Vet J 2006;84(1-2):30-35.

    36. Rutland B. New in the pipeline: Updates on feline IBD. Veterinary Information Network; 2010. http://www.vin.com/Members/CMS/Rounds/default.aspx?id=1144.

    37. Trepanier L. Idiopathic inflammatory bowel disease in cats: rational treatment selection. J Feline Med Surg2009;11(1):32-38.

    38. Davidson G. To benzoate or not benzoate: cats are the question. Int J Pharm Comp 2001;5(2):89-90.

    39. Sekis I, Ramstead K, Rishniw M, et al. Single-dose pharmacokinetics and genotoxicity of metronidazole in cats. J Feline Med Surg 2009;11(2):60-68.

    40. Olson EJ, Morales SC, McVey AS, Hayden DW. Putative metronidazole neurotoxicosis in a cat. Vet Pathol 2005;42(5):665-669.

    41. Henriksen M, Jahnsen J, Lygren I, et al. C-reactive protein: a predictive factor and marker of inflammation in inflammatory bowel disease. Results from a prospective population-based study. Gut 2008;57(11):1518-1523.

    42. Crandell JM, Jergens AE, Morrison JA, et al. Development of a clinical scoring index for disease activity in feline inflammatory bowel disease. J Vet Int Med 2006;20:788-789.

    43. Jergens AE. Controversies in canine/feline IBD II. Proc 79th Western Veterinary Conference 2007.

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