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Feline Inflammatory   Bowel Disease

Inflammatory bowel disease (IBD) is a chronic gastrointestinal tract disorder involving the proximal or distal portions of the gastrointestinal tract.  Clinical signs may vary depending upon the site of involvement.  As the pancreatic and biliary ducts are combined in cats, IBD may result in concurrent pancreatitis and cholangiohepatitis, called "triaditis".

Etiology:  The cause of IBD is not known, but thought to be the result of an appropriate immune response to a persistent, abnormal stimulus (luminal pathogen) or an abnormal, prolonged response to a normal stimulus (dietary protein and enteric microflora).  Improper immune response against enteric bacteria is proposed to be an essential co-factor.

Signalment and clinical presentation:  No gender, age, or breed predispositions exist for feline IBD.  Mostly middle to old-aged cats are affected, but IBD has also been diagnosed with some frequency in cats less than one year old.  Small intestinal IBD typically results in vomiting and weight loss whereas large intestinal IBD causes hematochezia.  Other clinical signs include lethargy, anorexia and ravenous appetite.  In cats with triaditis, icterus and palpable liver are seen.  Severity of the signs does not correlate well with the severity of the infiltrate and the site involved.

Diagnosis: Diagnosis of IBD is by histologic exam and exclusion of other causes of gastrointestinal inflammation.  Clinical differential diagnoses include:

a) Endocrine disease (hyperthyroidism,   exocrine pancreatic insufficiency)
b)  Food intolerance
c)  Infectious enteritis
d)  Chronic parasitism
e)  Neoplasia

Baseline tests:  Baseline laboratory tests should include complete blood count, serum biochemistry panel, urinalysis, serum free T4 concentration, FeLV/FIV test, fecal analysis (zinc sulfate flotation, direct smear, fecal wet mount, ELISA for antigen detection).  Changes in protein, liver enzymes, cholesterol, and potassium have been noted in affected cats.  Biochemical evidence for pancreatic and hepatic involvement may be seen in cats with triaditis.  Changes in the CBC are not specific, but hemoconcentration, leukocytosis, neutro-penia, eosinophilia and basophilia have been noted.

Imaging procedures:  Survey and contrast radiographs are not helpful in detecting IBD, but can be used to rule out other conditions (e.g. obstruction, intra-abdominal masses).  Ultrasound can be used to choose appropriate procedures (endoscopy or exploratory laparotomy) for the collection of a biopsy specimen.

Biopsy:  Histologic examination of the duodenum and colon is required for definitive diagnosis.  Endoscopic or full-thickness surgical biopsies may be used for histological evaluation.  It is important to obtain multiple tissue samples from each site and from different areas (e.g. duodenum, jejunum, ileum, colon) of the alimentary tract.  The limitations of endoscopy are that only mucosal biopsy can be performed (the disease could be deeper) and several areas of the digestive tract cannot be reached by this method.

  Full thickness biopsy may be warranted if endoscopic biopsies are nondiagnostic and other causes of vomiting and diarrhea have been ruled out.  If laparotomy is performed, biopsies of stomach, duodenum, jejunum, ileum, liver and pancreas should be obtained.  Full thickness colonic biopsies should be avoided (endoscopy is the preferred method for colon).

Histopathologic findings:  Increased numbers of inflammatory cells are present in the lamina propria.  Typically, all cell lines are present but the type of IBD is named for the predominant cell type.

  • Lymphoplasmacytic IBD is the most common form.  The lamina propria is infiltrated with lymphocytes and plasma cells

  • Eosinophilic IBD is the second most common form.  It is characterized as diffuse or focal infiltration of mature eosinophils into one or more layers of the intestinal tract.  This form of IBD may be one component of feline hypereosinophilic syndrome.

  • Suppurative forms of IBD are uncommon; when present, an infectious etiology should be investigated.

  • Regional granulomatous gastro-enteritis is rare and typically manifests as a thickened, partially stenotic segment of bowel.  This form must be differentiated from granulomatous inflammation caused by fungal disease, intestinal parasites, feline infectious peritonitis, viral infection, foreign material, toxoplasmosis, and neoplasia.

Other histologic findings include an increased number of intraepithelial lymphocytes and altered mucosal architecture (villous fusion or atrophy, edema, fibrosis, and dilation of lacteals).  The submucosa is not commonly affected, except in aggressive forms (e.g., eosinophilic and regional granulomatous gastroenteritis).

Grading IBD:  IBD is histologically graded into mild, moderate and severe, based on the severity of the inflammation in the biopsy sample (endoscopic and full thickness biopsy).

  • Mild: Inflammation without archi-tectural distortion

  • Moderate: Inflammation with separ-ation and distortion of glands or crypts and mild villous blunting

  • Severe: Inflammation with multifocal epithelial necrosis, marked separation of glands or crypts, fibrosis, and marked villous blunting and fusion

Dilemma:  A significant dilemma is to distinguish between severe lymphoplasmacytic gastroenteritis and early lymphosarcoma.  In these cases, immunohistochemical staining of lymphocytes can help to determine the phenotype of the infiltrating lymphocytes (monomorphic populations of lymphocytes are suggestive of lymphosarcoma).

Treatment:  Treatment is aimed at removing the antigenic source of inflammation and/or suppress the cell mediated inflammatory response in the gastrointestinal tract.

  • Nutritional therapy: The diet should contain a single, highly digestible, gluten-free, novel protein (the one that animal has not been previously exposed to) and reduced amounts of food additives.  High fat diets should be avoided.  If colitis is present, consider high fiber diets containing either insoluble or soluble fiber

  • Pharmacologic therapy:  Nutritional therapy alone for moderate to severe IBD is seldom successful and most animals require pharmacological therapy.

-by Kazuhisa Miyakawa, ECFVG Student

-edited by Dr. Vimala Vemireddi, ADDL Graduate Student


  1. Baez JL, Hendrick MJ, Walker LM, Washabau RJ: 1999.  Radiographic, ultrasonographic, and endoscopic findings in cats with inflammatory bowel disease of the stomach and small intestine: 33 cases (1990-1997). JAVMA 215:349-354.

  2. Carrens JK, Goldschmidt M, Lamb M, McLear RC, Drobatz KJ, Sorenmo KU: 2003.  Feline Epitheliotropic Intestinal Malignant Lymphoma: 10 cases (1997-2000).  J Vet Inter Med 17:326-331.

  3. Krecic MR: 2001.  Feline Inflammatory Bowel Disease: Pathogenesis, Diagnosis and Relationship to Lymphosarcoma.  Compen-dium 23: 951-961.

  4. Jergens AE: 2002.  Feline inflammatory bowel disease-current perspectives on etiopathogenesis and therapy.  J Fel Med and Surg 4: 175-178.

  5. Johns AJ: 2001.  Inflammatory Bowel Disease.  Feline Internal Medicine Secrets.  107-113.

  6. Magne ML: 1992.  Pathophysiology of Inflammatory Bowel Disease.  Seminars in Veterinary Medicine and Surgery (Small Animal) 7(2): 112-116.

  7. Tams TR: 1993.  Feline inflammatory bowel disease.  Vet Clin Nor Am: Small Anim Prac 23(3): 569-586.

  8. Weiss EJ, Gangne JM, Armstrong PJ: 1996.  Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats.  JAVMA 109(6): 1114-16.

  9. Willard MD: 1999.  Feline inflammatory bowel disease: A Review.  J Fel Med and Surg 1:155-164.



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