Histiocytic Colitis in Boxers and Other Large Bowel Disease
World Small Animal Veterinary Association World Congress Proceedings, 2007
Caroline Mansfield, BSc, BVMS, MVM, MACVSc, DECVIM-CA
Department of Veterinary Clinical Sciences, Murdoch University
Western Australia

The large intestine is responsible for absorption of water, sodium, chloride and short chain fatty acids, whilst it secretes potassium and bicarbonate. The colon has a physiological barrier (mucus layer) and a significant commensal bacteria population. Colonic bacteria produce short-chain fatty acids (SCFA), and this can contribute up to 10% of the animal's energy requirements. In dogs the majority of the colonic bacteria are anaerobes (90%), whilst in cats approximately half are anaerobic. Large intestinal diarrhea can occur by a number of mechanisms. In an otherwise normal colon without well-developed flora (e.g., neonates), excess sugars are not converted to SCFA and cause an osmotic diarrhea. In the normal colon with well-developed flora, but overloaded with readily fermentable carbohydrate, the luminal pH falls, lactic acid is produced, and osmotic diarrhea also develops. Diarrhoea may also occur if the large bowel is inherently diseased, and this may be independent of SI disease. Hallmark clinical signs of colonic inflammation or 'colitis' include (from most to least common):

 Mucoid faeces

 Tenesmus (straining to defecate)

 Haematochezia (fresh blood in the faeces)

 Mucoid faeces



 Rarely associated with weight loss, but vomiting can occur in cats

Differential Diagnosis for LI Diarrhoea (Colitis)

 Fibre-responsive/idiopathic colitis

 Inflammatory bowel disease:

 Lymphocytic-Plasmacytic Enteritis

 Histiocytic Ulcerative Colitis

 Eosinophilic colitis

 Granulomatous colitis

 Clostridial perfringens-associated diarrhoea

 Trichuris vulpis (whipworm)



 Adenocarcinoma (although haematochezia most prominent clinical sign)



 Irritable bowel syndrome

 Uraemic colitis

Animals presenting with colitis symptoms can be accurately diagnosed and successfully treated in most cases. A logical approach to diagnosis and a thorough understanding of possible pathogenesis in order to formulate a treatment trial is necessary to ensure this. Good and accurate history along with rectal examination is mandatory. Other investigations include faecal analysis, metabolic screening and either colonoscopy and biopsy or proctoscopy and biopsy. Full-thickness colonic biopsies are not indicated in most dogs with mild colonic signs. If no systemic or physical abnormalities are detected then a treatment trial could be used: faecal analysis or treatment with fenbendazole (50 mg/kg sid 3-5 days) and fibre supplementation (Metamucil). A failure to respond to treatment would then necessitate further investigation.

This treatment approach is not recommended in Boxer dogs presenting with colitis, as they are predisposed to a form of inflammatory bowel disease (IBD) called Histiocytic Ulcerative Colitis (HUC), although the disease has also been reported in other breeds. Typically affected dogs are usually less than 2 years old at presentation. The clinical signs of HUC are usually severe and often associated with weight loss or poor growth. Haematochezia is a prominent component. Diagnosis of HUC is based on histological documentation of a mucosal infiltrate of plasma cells, lymphocytes and Schiff-positive macrophages within the colon. Traditionally prognosis has been considered guarded when traditional immunosuppressive and dietary therapy has been used, although spontaneous resolution has been reported.1 There has however been a paradigm shift in the thinking about the pathogenesis of this disease, resulting in a different treatment approach. It appears that HUC is in fact an example of dysbiosis, where functionally distinct bacterial strains can lead to a form of IBD, and this new state of knowledge confers a much better prognosis for this disease.

Published reports have documented clinical resolution in dogs treated with enrofloxacin alone at 5 mg/kg/day for 6-8 weeks.2,3,4 Some of our dogs have now been disease-free for over 30 months following on treatment course. When this disease was first identified in the 1960's,5 an infectious aetiology was proposed and investigation concentrated on organisms such as Mycoplasma, but failed to identify a causative organism.6 Recent evidence about the immunological cell distribution present in the colonic mucosa of dogs with HUC7 correlates well with this new thinking about one possible pathogenesis of IBD. There is increasing evidence that suggests that IBD may be a consequence of an abnormally exuberant immune response to normal intestinal flora.8 This appears to occur in genetically susceptible individuals, and such an abnormal response may occur in the Boxer dog. Adherent and invasive E coli have been demonstrated to be present within the colonic mucosa of affected dogs, but not in controls.9,10 Comparisons can be made with spontaneous Crohn's disease in people, where an increased immune response to enteric bacteria occurs.11 It has further been established that these bacteria are no longer present following treatment with enrofloxacin (unpublished observation).

Fibre-responsive colitis is an idiopathic condition of dogs, in which clinical signs of colonic inflammation are present, but histological evaluation of colonic biopsies is unremarkable. This disease carries a good to excellent prognosis and responds well to soluble fibre supplementation or low-residue diets. Cats do not appear to be affected by this condition. Fibre supplementation may be beneficial by promoting colonic transit via stimulation of segmental contractions, altering the bacterial population in the lumen, increasing the production of SCFA or by absorbing large amounts of faecal water in its own right.

Lymphocytic-plasmacytic colitis may be part of a diffuse IBD in dogs, but is more common in cats as an isolated condition. Diagnosis is based on histopathology, and hypersensitivity is considered a possible cause in many cases. Initial treatment should consist of feeding a hypoallergenic or hydrolysed diet with added omega-3 fatty acids. If there is a poor response then fibre supplementation or a change to a low-residue diet may result in improvement. In rare cases immunosuppression (with prednisolone as for IBD) or sulfasalazine may be required. If animals are still refractory to this treatment increasing immunosuppression or considering the use of loperamide or probiotics may be of benefit. However, if this is necessary I think it is wise to reconsider the original diagnosis. Eosinophilic colitis is rare and generally always requires immunosuppression. Granulomatous colitis may also occur, but is extremely uncommon and often results in masses that may require surgical excision. In endemic areas elimination of infectious aetiologies is vital prior to starting the strong immunosuppression also required.

Colitisdue to C perfringens may a relatively common cause of colitis (and may also be associated with other intestinal signs such as vomiting).12 It is often triggered by stress such as a hospital stay, and there are suggestions it may actually be a nosocomial infection.13 Unfortunately this condition is notoriously difficult to diagnose as C perfringens is anormal colonic inhabitant and the use of toxin assay (RPLA), culture and faecal spore numbers has been shown to be unreliable at diagnosing this condition.14 Improved diagnostic sensitivity can be obtained by measuring C perfringens enterotoxin by ELISA in combination with PCR detection of enterotoxigenic strains in faeces after heat or alcohol shock treatment.15 It is controversial as to whether there is a necessity for antibiotics as fibre supplementation (to decrease colonic transit time and improve segmental contraction) may be the treatment of choice. Empirical antibiotic usage should be metronidazole or tylosin if required. C difficile has also been reported as a possible cause of nosocomial diarrhoea in cats, but its true pathogenesis is unknown.16

Pythiosis, protothecosis and histoplasmosis have all been reported to affect the colon and cause inflammation. The mucosa generally becomes quite nodular and there may be significant abdominal lymphadenopathy. Generally animals are significantly unwell with these conditions and diagnosis is based on demonstration of the organisms within the colonic mucosa as well as positive culture results. Generally these diseases should be considered only in highly endemic areas.

Irritable bowel syndrome (IBS) is commonly diagnosed in people, and may well be a significant cause of large intestinal signs in dogs, but it is virtually impossible to diagnose definitively in companion animals.17 IBS is a functional disorder causing deranged motility and abnormal pain perception. Clinical signs are often triggered by stress, and the condition has been associated with psychiatric illness in people. The hallmark clinical signs in dogs are mucoid diarrhoea, increased faecal frequency, signs of faecal urgency or abdominal discomfort. IBS can only be diagnosed in dogs by complete exclusion of all other organic intestinal disease that can produce similar clinical signs. Confidence in your diagnosis must be present as individual dogs have varying responses to treatment is variable and clients may become frustrated if they are not led to expect this. Treatment consists of a combination of dietary manipulation (fibre supplementation to improve normal motility), reduction of environmental stressors, motility modifiers such as loperamide and anti-spasmodic agents.


1.  Churcher & Watson (1997) Canine histiocytic ulcerative colitis. AVJ 75:710-713

2.  Davies et al (2004) Successful management of histiocytic ulcerative colitis with enrofloxacin in two Boxer dogs. AVJ 82:50-54

3.  Hostutler et al (2004) Antibiotic-responsive histiocytic ulcerative colitis in 9 dogs. JVIM 18:499-504

4.  Mansfield et al (2004) Resolution of histiocytic ulcerative colitis in six boxers. ECVIM Congress Proceedings

5.  Van Kruiningen et al (1965) A granulomatous colitis of dogs with histologic resemblance to Whipple's disease. Pathol Vet 2:521-544

6.  Bowe et al (1982) Attempts to produce granulomatous colitis in Boxer dogs with a Mycoplasma. Can J Comp Med 46:430-433

7.  German et al (2000) An immunohistochemical study of histiocytic ulcerative colitis in boxer dogs. J Comp Path 122:163-175

8.  Swidsinski et al (2002) Mucosal flora in inflammatory bowel disease. Gastroenterology 122:44-54

9.  Simpson et al (2006) Adherent and Invasive Escherichia coli is associated with granulomatous colitis in boxer dogs. Infection and Immunity 74: 4778-4792

10. Van Kruiningen et al (2005) The comparative importance of E. coli antigen in granulomatous colitis of Boxer dogs. APMIS 113:420-425

11. Darfeuille-Michaud et al (2004) High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn's disease. Gastroenterology 127:412-421

12. Weese J, et al. (2001) The roles of Clostridium difficile and enterotoxigenic Clostridium perfringens in diarrhea in dogs. JVIM 15: 374-378.

13. Kruth SA et al.(1989) Nosocomial diarrhea associated with enterotoxigenic Clostridium perfringens infection in dogs. J Am Vet Med Assoc 195: 331-334.

14. Marks S, et al. (1999) Evaluation of methods to diagnose Clostridium perfringens-associated diarrhea in dog JAVMA 214: 368-371

15. Marks & Kather (2006) In: Greene (Ed) Infectious Diseases of the Dog, 3rd edition pp 363

16. Madewell et al (1998) Clostridium difficile in a survey of fecal carriage in cats in a veterinary teaching hospital J Vet Diagnostic Investigations 11:50-54

17. Tams TR. (1992) Irritable bowel syndrome. In: Kirk RW, Bonagura JD (ed.). Current Veterinary Therapy XI. Philadelphia, W B Saunders Company, 1992; 604-608.

Speaker Information
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Caroline Mansfield, BSc, BVMS, MVM, MACVSc, DECVIM-CA
Murdoch University
Western Australia, Australia

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