Approach to Canine and Feline Colitis
World Small Animal Veterinary Association World Congress Proceedings, 2010
Iwan A. Burgener,, PhD, DACVIM, DECVIM-CA
Bern, Switzerland

Read the German translation: Kolitis Beim Hund


Colitis is defined as inflammation of the colon and is the most common cause of large bowel diarrhea. The colon plays an important role in conservation of water and electrolytes and is the major site of fecal storage until expulsion is necessary. In regard of digestion and metabolism, the colon is often underestimated. The colonic bacterial flora plays an important role in the fermentation of undigested carbohydrates with the primary substrate dietary fiber. Disruptions of the normal homeostasis of the colon may lead to changes in both the absorption and motility. Clinically this is often manifested as large bowel diarrhea.1


Normal intestinal epithelium is not inflamed despite close contact with a high density of commensal organisms. Intestinal epithelial cells are not only a barrier between the body and viruses, bacteria, and parasites present in the intestinal lumen, but are also immunologically active through antigen processing and presentation, secretion of cytokines, and recruitment of inflammatory cells in response to pathogens.2 Inflammatory bowel disease (IBD) is believed to result from predisposing genetic factors and environmental stimuli such as microbe-associated molecular patterns being recognized by the host immune system and causing inflammation of the gastrointestinal mucosa.3 In dogs with IBD, the breakdown of immunologic tolerance to luminal antigens (bacteria and dietary components) is thought to be critical, perhaps resulting from disruption of the mucosal barrier, dysregulation of the immune system, or disturbances in the intestinal microflora.4

Inflammation of the colon reduces the amount of water and electrolytes absorbed and changes colonic motility. Cytokines produced alter smooth muscle function, resulting in abnormal motor activity. Inflammation suppresses the normal colonic contractions that mix and knead, and stimulates giant migrating contractions (GMCs). GMCs are more powerful contractions that rapidly propel intestinal contents. These contractions only occur once to twice daily, but colonic inflammation increases the number of daily GMCs. It is believed that they are a major factor in producing diarrhea, abdominal cramping, and increased urgency associated with colitis. Goblet cells respond to inflammation by producing increased amounts of mucus.1


Histology may be a helpful tool especially in chronic colitis, even though the lack of standardization was a problem up to now. Hopefully, this will change with the new WSAVA standardization.5 Colitis is usually defined histologically by the predominant inflammatory cell type present, the alterations of the normal colonic architecture and the severity of the disease.1

Lymphocytic-plasmacytic colitis is the most common form of colitis in both the dog and cat. There may be an association between colitis in dogs and perianal fistulas, especially in the German shepherd dog, whereas purebred cats are affected more often than non-purebred cats. Most lymphocytes and plasma cells are in the lamina propria and crypt dilatation, loss of surface epithelial cells, and decreased goblet cells are other histopathologic changes associated with chronic colitis.

Eosinophilic colitis is characterized by accumulations of eosinophils in the lamina propria. The patients may reveal a peripheral eosinophilia which may be one component of the hypereosinophilic syndrome. This form occurs uncommonly, and the animals affected tend to be younger. Endoparasites, infectious agents, and food allergy have all been incriminated in this form of colitis, but none have been proven. Regardless, it is prudent to investigate and eliminate these potential etiologies first since treatment of eosinophilic colitis tends to be more difficult than that of lymphocytic-plasmacytic colitis.

Granulomatous colitis is characterized by the presence of not periodic acid-Schiff (PAS) positive macrophages and other inflammatory cells within the lamina propria. Granulomatous colitis is rare and usually presents as a segmental, thickened, partially obstructed segment of bowel. The ileum and colon appear to be affected most commonly. It is important to eliminate inflammation secondary to fungal disease, intestinal parasites, feline infectious peritonitis, and foreign material.1 Treatment remains controversial, although most advocate surgical resection if possible.

Histiocytic ulcerative colitis (HUC) is a severe inflammatory disease that typically affects boxer dogs under 4 years of age. Other breeds such as French bulldogs, mastiff, Alaskan malamute, and Doberman pinscher are affected sporadically.6,7 Accumulation of PAS-positive macrophages and loss of epithelium and goblet cells lead to thickening and ulceration of the colon and subsequently bloody mucoid stools, anemia, hypoalbuminemia, and weight loss. Until recently, HUC was considered a special form of IBD, but an adherent and invasive phenotype of E. coli was discovered as the etiologic agent of the disease.6 This explains why enrofloxacin for at least 4-6 weeks is the treatment of choice for this disease.8

Differential Diagnosis

Whereas symptomatic treatment may be sufficient for some cases of acute colitis, it is important to obtain a definitive diagnosis for any animal that has chronic large bowel diarrhea. Since the clinical signs of chronic colitis are similar to those of other disease of the large bowel, it is important to perform diagnostics to establish a diagnosis.





Trichuris vulpis and others

Tritrichomonas foetus and others


Clostridium perfringens
Enteroinvasive E.coli (HUC)

Clostridium perfringens


Histoplasma capsulatum
Pythium insidiosum



Food hypersensitivity

Food hypersensitivity


Adenocarcinoma, lymphoma
Adenomatous polyps

Adenocarcinoma, lymphoma

Clinical Signs and Physical Examination

The most common clinical sign of colitis is large bowel diarrhea. The characteristics of large bowel diarrhea include mucus, hematochezia, tenesmus, and occasionally pain when defecating. Furthermore, there is often an increased urgency and frequency of defecation, but the amount of feces per bowel movement is greatly reduced. In cats with chronic colitis, hematochezia without diarrhea may be the most common clinical sign. Vomiting and weight loss can occur, but these tend to be the more severe cases (e.g., HUC) or those that have concurrent disease that also affect the stomach or small intestine.

The history may reveal a waxing and waning course of clinical signs that may be sporadic initially, but progression usually occurs and may lead to persistent disease. The physical examination is usually within normal limits. In severe cases or cases with concurrent disease, poor body condition suggestive of weight loss may be found. Every patient with signs of colitis should have a rectal examination performed as it may reveal an irregular or thickened mucosal surface, elicit pain, and demonstrate frank blood or mucus on the examination glove. In addition, a thorough rectal examination may discover a rectal polyp or malignant neoplasm which can mimic the signs of chronic colitis.

Diagnostic Plan

The diagnostic approach for chronic cases should be systematic and thorough and may include colonic biopsies. Initially it is important to exclude all other disease that can mimic the signs of chronic colitis. Multiple fecal exams (3x native, 3x zinc sulfate) should always be performed. Especially T. vulpis (dogs; fecal flotation) and T. foetus (cats; direct smear, in pouch culture, PCR) commonly cause large bowel diarrhea. Rectal cytology is an invaluable diagnostic tool. Specimens can be collected using a glove, a moistened cotton swab, or conjunctival spatula (epithelial cells exfoliate easily). Normal cytology reveals colonic epithelial cells, a mixed population of bacteria and yeast, and some debris. Abnormal findings include inflammatory cells, neoplastic cells, and certain intracellular infectious organisms (e.g., H. capsulatum) or a large number of clostridial endospores. However, cases of suspected clostridial colitis should be confirmed by identifying C. perfringens enterotoxins A and B in feces using a commercially available ELISA or PCR after a bacterial culture.

Dietary trials can be performed before pursuing more advanced diagnostics such as colonoscopy. A highly digestible diet like i/d (Hill's), Intestinal (Royal Canin), EN (Purina) or Low Residue (Eukanuba) possibly supplemented with soluble fiber (e.g., psyllium) for at least 4-6 weeks is a good choice. Psyllium (Metamucil) at 1.33 g/kg per day resulted in favorable response in greater than 85% of patients with chronic idiopathic large bowel diarrhea. Soluble fibers hold water, thereby improving the consistency of feces, stabilizing colonic motility, and altering colonic bacterial metabolism. In regard to food hypersensitivity and IBD, a novel protein or hydrolyzed diet can also improve the clinical signs to reflect colonic involvement in most cases with food-responsive diarrhea (FRD) in dogs and cats.9,10

If the signs persist, further diagnostics are indicated. A CBC, chemical profile and urinalysis should be performed but are normal in the majority of cases. For cats, FeLV/FIV testing is recommended, as well as T4 if indicated based on the cat's age. Routine abdominal radiographs are usually normal but occasionally demonstrate intraluminal narrowing, which could indicate an infiltrative disease process with luminal obstruction (often seen with lymphomas in cats and pathologic strictures in dogs). Abdominal ultrasound may help with the assessment of the mucosal layers as well as identifying infiltrative processes. Finally, colonoscopy is indicated to visually inspect the mucosal surface and obtain biopsies for histopathology. Patient preparation is essential in obtaining a reliable examination when small or subtle lesions could be missed by residual fecal material. Multiple samples from the caecum, ascending, transverse, and descending colon should be obtained regardless of the gross morphologic appearance. Difficulty lies with differentiating histologically normal mucosa from mild colitis and severe inflammatory lesions from lymphoma.


There is little evidence-based medicine in the veterinary literature regarding the management of chronic colitis. Most therapeutic protocols include a combination of dietary and pharmacological intervention, and the choices are often clinician-dependent. Most treatments should continue for 2-4 weeks past resolution of clinical signs before initiating dose reduction of the medications given. Independent of the clinical improvement, most dogs with IBD or FRD do not show significant improvements of histopathologic lesions.9,10 Because of the intermittent shedding of ova by whipworms, empiric deworming is recommended even if the results of the fecal exam are negative (e.g., fenbendazole, 50 mg/kg po q24h for 3 days; potentially repeated after 3 weeks and 3 months).

Nutritional management

Highly digestible diet +/- psyllium

Novel protein diet / hydrolyzed diet



20-30 mg/kg PO q8h (dog)
10-20 mg/kg PO q24h (cat)

Olsalazine, mesalamine

10-20 mg/kg PO q8h (dog)



1-2 mg/kg PO q12h (dog, cat)
tapering after resolution of signs


1-3 mg/kg PO q24h (dog)
1 mg/kg PO q24h (cat)


5 mg/kg PO q24h (dog)


2 mg/kg PO q48h (cat)


2 mg/kg PO q24h (dog)



10-20mg/kg PO q12h (dog, cat)


10-40 mg/kg PO q12h (dog, cat)


5-10 mg/kg PO q24h (dogs with HUC)


1.  Parnell NK. 2009; Kirk's Current Veterinary Therapy XIV: 515.

2.  Hershberg RM, et al. Immunol Today 2000;21:123.

3.  Isaacs KL, et al. Inflamm Bowel Dis 2005;11(Suppl 1):S3.

4.  German AJ, et al. J Vet Intern Med 2003;17:8.

5.  Day MJ, et al. J Comp Path 2008;138:S1.

6.  Simpson KW, et al. Infect Immun 2006;74:4778.

7.  Simpson KW. 2009; Kirk's Current Veterinary Therapy XIV: 521.

8.  Hostutler RA, et al. J Vet Intern Med 2004;18:499.

9.  Burgener IA, et al. J Vet Intern Med 2008;22:553.

10. Allenspach K, et al. J Vet Intern Med 2007;21:700.


Speaker Information
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Iwan A. Burgener, Dr., PhD, DACVIM, DECVIM-CA
Bern, Schweiz