Diagnosis
Chronic enteropathies are frequently encountered in dogs and cats, resulting in diarrhea and occasionally vomiting (Allenspach et al. 2007). The clinician faced with a case usually performs an extensive workup to exclude extra-gastrointestinal causes for diarrhea and vomitus (e.g., liver, kidney, hypoadrenocorticism (dogs), hyperthyroidism (cats)) as well as disorders such as pancreatic diseases, chronic parasitic or bacterial infections, and tumors.
Diagnostics performed to rule out underlying disorders include a complete blood count (CBC), serum biochemical analysis (incl. bile acids/ ammonium), urinalysis, hormonal testing(ACTH stimulation test in dogs, T4 in cats), parasitic and bacterial analysis of fecal samples, abdominal ultrasonography, and assessment of serum concentration of trypsin-like immunoreactivity (TLI), pancreatic specific lipase (PLI), serum cobalamin and folate concentrations. If there is no obvious underlying infectious, parasitic, pancreatic, neoplastic, endocrinologic or metabolic disease identified, these animals are mostly undergoing a trial therapy +/- endoscopy and are retrospectively diagnosed by the response to treatment as antibiotic-responsive diarrhea (ARD; Tylo sin-responsive chronic diarrhea (Westermarck et al. 2005); nowadays better dysbiosis), food-responsive diarrhea (FRD) or inflammatory bowel disease (IBD; also called steroid-responsive diarrhea).
Investigation of the intestinal microflora in dogs with IBD is difficult. One attempt to non-invasively assess the impact of the intestinal microflora is the measurement of serum cobalamine and folate concentrations. Cobalamine is absorbed via a receptor-mediated mechanism in the terminal ileum, and folate is absorbed in the jejunum. Theoretically, the increased number of bacteria should increase the serum level of folate and decrease the levels of cobalamine, because bacteria synthesize folate and bind cobalamine.
However, the sensitivity and specificity of these measurements are low (sensitivity 5-30%, specificity 30-100%; German et al. 2003). Molecular methods, such as molecular fingerprinting or pyrosequencing to detect bacteria in the duodenal juice or in biopsies will possibly be helpful to understand the impact of the microflora on disease mechanism in the future (Xenoulis et al. 2008).The diagnosis of IBD therefore involves careful integration of signalment (for breed predispositions see Simpson and Jergens 2011), home environment, history, physical findings, clinicopathologic testing, diagnostic imaging, and histopathology of intestinal biopsies. Furthermore, IBD is associated with histopathology evidence of inflammation in the intestinal mucosa with the infiltration of the gastric, small and/or large intestinal wall with inflammatory cells. The nomenclature reflects the predominant cell types present, with lymphocytic-plasmacytic enteritis (LPE) being the most commonly reported form. Most lymphocytes and plasma cells are in the lamina propria and crypt dilatation and loss of surface epithelial cells are often associated with this form. Eosinophilic (gastro-) enteritis is less common. 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, but none have been proven. Regardless, it is prudent to investigate and eliminate these potential etiologies first since treatment of eosinophilic enteritis tends to be more difficult than that of LPE. Granulomatous enteritis 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. Treatment of this form remains controversial, although most advocate surgical resection if possible.