Colitis

What it is

Colitis is inflammation of the colonic mucosa, which reduces the colon's capacity to absorb water and store faeces and increases mucus secretion. It is a clinical and histological description, not a single disease:

• Acute colitis: dietary indiscretion or sudden diet change, stress, parasites (Trichuris vulpis, Giardia), bacterial causes (Clostridium perfringens enterotoxin is suspected in some cases) and drugs. It is usually self-limiting.
• Chronic colitis (more than about three weeks): food-responsive enteropathy, antibiotic-responsive enteropathy, immunosuppressant-responsive enteropathy (inflammatory bowel disease, usually lymphoplasmacytic), fibre-responsive large-bowel diarrhoea, chronic parasitism and, in boxers and French bulldogs, granulomatous (histiocytic ulcerative) colitis associated with invasive Escherichia coli. Neoplasia (adenocarcinoma, lymphoma) and colorectal polyps must be ruled out.

Who it affects

Dogs of any age. Acute colitis is very common in young dogs and after dietary changes or kennel stays. Granulomatous colitis affects young boxers and French bulldogs.

Anatomy involved

• Large intestine: caecum, colon and rectum. The colon absorbs water and electrolytes and stores faeces; its inflamed mucosa loses absorptive capacity, produces more mucus and becomes irritable, so the rectum signals urgency even when it holds little faeces.
• In granulomatous colitis the mucosa is thickened, irregular and ulcerated, with macrophages laden with PAS-positive material in the lamina propria.

Clinical signs

Large-bowel diarrhoea: increased frequency with small volumes each time, urgency, mucus, fresh blood (haematochezia) and tenesmus. Weight loss is uncommon (it is more typical of small-bowel disease), although some dogs with colitis also vomit. Chronic cases may be intermittent.

Diagnosis

• Faecal examination (flotation, Giardia antigen) and empirical deworming, for example with fenbendazole.
• Rectal examination: mucosal irregularity, masses, pain, and assessment of the prostate and anal sacs.
• Blood work and abdominal imaging in chronic cases to exclude systemic disease and neoplasia; ultrasound assesses wall thickness and lymph nodes.
• Treatment trials: diet (hydrolysed or novel protein, or added fibre) before more invasive tests.
• Colonoscopy with biopsies: in chronic cases that do not respond; histopathology characterises the inflammation and excludes neoplasia; culture and fluorescence in situ hybridisation for granulomatous colitis.

Treatment

Acute colitis: a short period of a highly digestible diet, soluble fibre (such as psyllium) and treatment of parasites; antibiotics are generally not needed. Chronic colitis is treated stepwise: dietary trial (hydrolysed or novel protein, high-fibre diet), then probiotics, and immunosuppressants (prednisolone, budesonide, ciclosporin) when diet fails and biopsies support inflammatory bowel disease. Granulomatous colitis responds to antibiotics chosen by susceptibility testing, classically enrofloxacin. The prognosis is good for acute and diet-responsive forms.

In the cat

In the cat acute colitis has causes similar to those in the dog (diet changes, stress, Giardia, Cryptosporidium). A cause specific to the cat is Tritrichomonas blagburni (formerly called T. foetus), a flagellated protozoan that causes chronic large-bowel diarrhoea, malodorous, sometimes with fresh blood and mucus and even faecal incontinence, in young cats from catteries and shelters, often pedigree cats. It is diagnosed by a direct smear of fresh faeces, specific culture or, more sensitively, PCR; the treatment is ronidazole, which can cause neurotoxic effects and must be handled carefully, and in many cats the diarrhoea resolves on its own within months even though the infection persists.

Feline chronic enteropathy often affects the small and large intestine together, and many cats respond to a hydrolysed or novel protein diet; soluble fibre helps in large-bowel diarrhoea. In older cats colonic neoplasia (adenocarcinoma, lymphoma, mast cell tumour) must be ruled out, and overflow diarrhoea from severe constipation or megacolon must not be mistaken for colitis.

Key studies in the cat

Tritrichomonas

• Walden et al. (2013) described the feline parasite as a new species, Tritrichomonas blagburni, based on cross-infection experiments between cats and cattle, its different pathogenicity in each host and genetic differences from the bovine T. foetus.
• Gookin et al. (2006), in vitro testing plus treatment of 1 naturally and 10 experimentally infected cats. After ronidazole at 10 mg/kg, infection relapsed in all 5 experimental cats; at 30–50 mg/kg every 12 hours for 14 days, all 10 cats stayed PCR-negative for 21–30 weeks. Experimental infection in few cats.
• Foster et al. (2004), prospective follow-up of 26 cats with diarrhoea caused by T. foetus. Diarrhoea resolved in 23 cats a median of 9 months after onset, but 12 of the 22 cats retested were still infected a median of 39 months after the diarrhoea ended.
• Xenoulis et al. (2013), retrospective study of 104 PCR-positive pet cats. 98% had diarrhoea, with a median duration of 135 days. Of the 45 cats that completed ronidazole treatment, 64% responded well and the rest improved only partly, did not improve or relapsed soon after.

Diet in chronic enteropathy

• Guilford et al. (2001), 55 cats with chronic idiopathic gastrointestinal signs fed a selected-protein elimination diet. 29% were confirmed as food-sensitive on dietary challenge and another 20% improved without relapsing on challenge. In the food-sensitive cats, large-bowel diarrhoea was more common than small-bowel diarrhoea.
• Kathrani et al. (2020), primary-care records of 977 cats given a hydrolysed diet for chronic vomiting or diarrhoea. Response was poor in 34% of cats started on the diet alone and in 61% of those also given antibiotics or corticosteroids, and cats over 6 years old were more likely to respond poorly. Observational data without a confirmed diagnosis.