Eosinophilic enteritis (EE) is reported to be the second most common form of inflammatory bowel disease. It frequendy also involves the stomach and / or colon in eosinophilic gastroenteritis (EGE) and / or colitis. Segmental eosinophilic enteritis has also been reported. Histologically, variable mucosal architectural disturbances (e. g., villus atrophy) are present in conjunction with a mixed infiltrate of inflammatory cells in which eosinophils predominate. However, as with lymphocytic-plasmacytic enteritis, diagnostic criteria vary among pathologists; some define eosinophilic enteritis based purely on subjective increases in mucosal eosinophil numbers, whereas others apply stricter criteria, requiring that eosinophils predominate in the lamina propria. Another criterion is the presence of eosinophils between epithelial cells of the villus and crypt, which suggests transepithelial migration. Nevertheless, the number of mucosal eosinophils can vary markedly in normal dogs, and therefore this condition may be overdiagnosed. As with other forms of inflammatory bowel disease, a diagnosis of eosinophilic enteritis should be made only after other causes of eosinophiiic infiltration have been eliminated.
Eosinophilic enteritis may be seen in dogs and cats of any breed and age, although it is most common in younger adult animals. Boxers and Dobermans may be predisposed, and an increased incidence in German shepherds has been suggested. Eosinophilic gastroenteritis may also be associated with systemic eosinophiiic disorders in both cats and dogs. The clinical signs reported, which depend on the area of gastrointestinal tract involved, include vomiting, small intestine diarrhea, and large intestinal diarrhea. Mucosai erosion / ulceration may occur more frequendy in eosinophilic enteritis than in other forms of inflammatory bowel disease, therefore hematemesis, melena, or hematochezia may be seen. Severe EGE has been associated with protein-losing enteropathy and hypoproteinemia and, rarely, spontaneous perforation of the gastrointestinal tract.
An eosinophiiic mucosai infiltrate may be related to dietary sensitivity, endoparasitism, or idiopathic eosinophilic gastroenteritis. The eosinophil infiltration is likely to be the result of local and systemic production of cytokines and chemokines, such as IL-5, and members of the eotaxin family. These mediators may be produced by the Th2 subset of CD4+ T cells.
The diagnosis of eosinophilic gastroenteritis is made by histopalhologic assessment of intestinal biopsies after exclusion of parasites and food allergy. Peripheral eosinophilia is neither invariably present nor pathognomonic for eosinophilic gastroenteritis, because it may also be seen in parasitism, hypoadrenocorticism, allergic cutaneous or respiratory disease, and mast cell neoplasia.
Given that eosinophilic mucosai infiltrates may also be related to endoparasitic diseases, empirical treatment with fenbendazole is always advisable. Subsequent to this, an exclusion diet trial should be instigated to eliminate the possibility of dietary sensitivity before immunosuppressive therapy is considered. The prognosis in idiopathic eosinophilic gastroenteritis is guarded, even with a good initial response to treatment, because recurrence is common.