Canine Colitis

Chapter 134


Canine Colitis




The term colitis frequently is used to describe the clinical syndrome characterized by bloody mucoid diarrhea and tenesmus, or dyschezia, presumed to be caused by inflammation of the colonic mucosa. The modifiers acute and chronic are used to describe the chronicity of clinical signs. However, a definitive diagnosis of colitis requires histopathologic examination of the colonic mucosa. Thus a clinical diagnosis of “acute colitis” rarely is confirmed by colonic biopsy because most patients do not require endoscopy and respond to conventional therapy. Conversely, a clinical diagnosis of “chronic colitis” always should be confirmed by histopathology, because the success of treatment is related closely to the histopathologic appearance. This chapter reviews the diagnosis and treatment of canine colitis with an emphasis on the management of lymphoplasmacytic and granulomatous colitis.



Diagnostic Approach


The diagnostic approach to dogs presenting with signs of colitis is directed at detecting or ruling out extracolonic causes of tenesmus, dyschezia, or fresh blood in the feces, such as prostatomegaly, perineal hernia, constipation, pelvic canal abnormalities, anal sac and perianal problems, and the various causes of large bowel diarrhea (Table 134-1).



In dogs with acute signs of large bowel diarrhea, the diagnostic plan typically consists of fecal examination for parasites (Giardia spp., whipworms), fecal culture (Campylobacter and Salmonella spp., with or without Clostridium spp.), and possibly fecal ELISA for Clostridium toxins. Acute colitis frequently responds to symptomatic therapy with anthelminthics (e.g., fenbendazole) or diet.


If the dog is systemically unwell, or large bowel diarrhea is severe or chronic, a biochemical profile, urinalysis, and complete blood count should be submitted to screen for systemic disease. Rectal cytology can be informative in detecting fungi (Histoplasma spp.) and ingested bacteria within neutrophils. Survey radiographs of the abdomen often yield little information about primary colonic disease but can be performed to screen for masses or foreign bodies and to evaluate the relationship of the colon to other viscera and the pelvic canal. Ultrasonography is useful for ruling out extracolonic causes of large bowel diarrhea, detecting ileocecocolic lesions, and assessing mural infiltration of masses and regional lymph nodes. In many animals with large bowel diarrhea the physical exam, fecal exam, laboratory testing, and imaging are normal, enabling the problem to be localized to the large bowel. The next step in the investigation of large bowel diarrhea is colonoscopic examination of the rectum, colon, and cecum and, if indicated, the terminal ileum (e.g., concurrent signs of small bowel diarrhea or low serum cobalamin). Principal differential diagnoses at this stage include inflammatory bowel disease, polyps, and neoplasia. At least 8 to 10 endoscopic biopsies of normal and abnormal mucosa should be acquired for histopathologic evaluation because lesions can be patchy. Where granulomatous colitis is suspected (see granulomatous colitis later), biopsies should be obtained for bacterial culture. Rigid proctoscopy is an alternative to flexible endoscopy for investigating and biopsying the distal colon and rectum.



Histopathologic Features of Colitis


A definitive diagnosis of colitis is based on histopathologic evaluation of colonic biopsies. Colitis falls under the umbrella term inflammatory bowel disease (IBD), which usually is defined by increased cellularity of the lamina propria. The extent of colonic inflammation varies from focal to diffuse involvement. The type and degree of cellular accumulation is also variable and is categorized subjectively as normal, mild, moderate, or severe.


Increased numbers of lymphocytes and plasma cells, so-called “lymphoplasmacytic enteritis,” is the most frequently reported form of colitis.


Colonic infiltration with macrophages or neutrophils is less common and raises the possibility of an infectious process, and culture, special staining, and fluorescence in situ hybridization (FISH) are indicated. The presence of moderate-to-large numbers of eosinophils in intestinal biopsy samples, often accompanied by circulating eosinophilia, suggests possible parasitic infestation or dietary intolerance.


The emphasis on cellularity has meant that abnormalities in mucosal morphology have been somewhat overlooked. Crypt hyperplasia often is interpreted as a regenerative response to an inflammatory stimulus. Erosions, ulcers, and fibrosis are interpreted to infer colitis of increased severity. A major problem of histopathologic evaluation is the subjectivity and variability of reporting. The recent finding that the WSAVA standardization of pathology scheme, like previous standardized photographic schemes, has poor agreement among pathologists, questions further the ability of standardized grading in its current form to translate to improved diagnosis and management of patients with IBD. A further limitation of the WSAVA scheme in respect to colitis is that it does not consider goblet cells, which correlate with the presence of granulomatous colitis and severity of lymphoplasmacytic colitis and show dramatic increases after treatment. Clearly, the emphasis on histopathologic evaluation has to shift from the subjective reporting of cellularity toward identifying and reporting features that correlate with presence of disease and its outcome. Although histopathologic changes can be helpful, they frequently represent a common endpoint of many different diseases.



Management of Chronic Colitis



Lymphocytic Plasmacytic Colitis


The predominant form of chronic colitis in dogs is characterized by mucosal infiltration with lymphocytes and plasma cells and frequently is referred to as lymphocytic plasmacytic colitis. The cause of lymphocytic plasmacytic colitis has not been determined, but it is suspected that intestinal inflammation in dogs, like people, is a consequence of uncontrolled intestinal inflammation in response to a combination of elusive environmental, enteric microbial, and immunoregulatory factors in genetically susceptible individuals.


Analysis of mucosal immunopathology has shown canine lymphocytic plasmacytic colitis is associated with an increase in CD3+ T cells, IgA and IgG, plasma cells, and up-regulation of proinflammatory cytokines interleukin-2 (IL-2) and tumor necrosis factor-α (TNF-α). There is currently no information on genetic susceptibility of dogs to lymphocytic plasmacytic colitis. In a recent study the authors sought to examine the relationship of mucosal bacteria to lymphocytic plasmacytic colitis in 23 dogs (unpublished observations). The authors observed numerous spiral bacteria inhabiting the mucus and glands of the healthy and inflamed colon that were consistent with enterohepatic Helicobacter spp. Findings included no evidence of Brachyspira spp., a decrease in the total number of mucosal bacteria, and a reduction in the proportion of Clostridium spp. relative to total bacteria and Enterobacteriaceae. These findings parallel the “dysbiosis” that is described in small intestinal IBD in dogs and establish that the density and composition of the colonic mucosal flora is related to the presence and severity of lymphocytic plasmacytic colitis in dogs (see Chapter 131). The authors observed a correlation between goblet cells, mucosal bacteria, and the histologic severity of colitis. The loss of mucus and goblet cells may be related to the dysbiosis associated with colitis. However, it is not clear if the microbial shifts are a cause or a consequence of inflammation, and their role in the etiopathogenesis of colitis has not been established.



Treatment


Studies in dogs with lymphocytic plasmacytic colitis provide reasonable evidence that various subsets of dogs respond to treatment with diet, antibiotics, or immunosuppressive therapy (Box 134-1). At present, because there is no reliable means for predicting which dogs will respond to which treatment, standard treatment consists of a series of therapeutic trials.



Box 134-1   Medical Management of Colitis


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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Canine Colitis

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