Eosinophilic enteritis (EE)
EE is reported to be the second most common form of IBD after LPE. It frequently involves the stomach (eosinophilic gastroenteritis, EGE), colon (eosinophilic enterocolitis, EEC), or both (eosinophilic gastroenterocolitis, EGEC).
In addition, segmental EE has also been reported.58 Histopathologically, variable mucosal architectural disturbances (e.g., villus atrophy) are present in conjunction with a mixed infiltrate of inflammatory cells with eosinophils predominating (Figure 9.8b). However, as with LPE, the diagnostic criteria vary between pathologists. The definition of EE may be based on subjective increases in mucosal eosinophil numbers despite increases in other inflammatory cells. More strict criteria require eosinophils to predominate in the LP. Other criteria include the presence of eosinophils between the epithelial cells of the villus and crypt, suggesting transepithelial migration. Nevertheless, there can be marked variation in the number of mucosal eosinophils in normal dogs and therefore this condition may be over-diagnosed.12 As with other forms of IBD, a diagnosis of EE should only be made once other causes of eosinophilic infiltration have been eliminated. Parasitic and allergic diseases should always be considered as possible differential diagnoses.Clinical signs
The condition can be seen in dogs and cats of any breed and age, although it is most common in younger adult animals. Boxers, German Shepherds, and Dobermans may be predisposed. EGE may also be associated with systemic eosinophilic disorders (i.e., hypereosinophilic syndrome) in both cats and dogs. The clinical signs reported depend on the area of the GI tract involved, and include vomiting, SI diarrhea, and LI diarrhea. Hematemesis, melena, or hematochezia may be seen as mucosal erosion and /or ulceration may occur more frequently in EE than in other forms of IBD.
Severe EGE has rarely been associated with spontaneous perforation of the GI tract, but PLE and hypoproteinemia are commonly recognized.59Pathogenesis
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.60 An eosinophilic mucosal infiltrate may be caused by dietary sensitivity, endoparasitism, or idiopathic EGE.
Diagnosis
The diagnosis of EGE is made by histopathological assessment of intestinal biopsies, and after exclusion of parasites and food allergy. Peripheral eosinophilia is neither pathognomonic for nor invariably present in EGE. It is probably more commonly seen in parasitism, hypoadrenocorticism, allergic cutaneous or respiratory disease, and mast cell neoplasia.
Treatment
Given that eosinophilic mucosal infiltrates may also be related to intestinal parasitism, empirical anthelmintic and antiprotozoal treatment is always advisable initially. If there is no response to treatment, a dietary trial with an exclusion diet should be instigated to eliminate the possibility of dietary sensitivity before considering immunosuppressive therapy. The prognosis for patients with idiopathic EGE is guarded, even with a good initial response to treatment, as recurrence is common.
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