Eosinophilic enteritis (EE) has been reported to be the second most prevalent variant of inflammatory bowel disease (IBD), only surpassed by the lymphocytic-plasmacytic form.51 Although the etiology is poorly defined, it has been hypothesized that affected cats suffer from immunologic dysregulation triggered by one or more factors, possibly including food ingredients (eg, food allergies or intolerance), dysbiosis of gut microbiota, or other factors (eg, ingestion of ectoparasites, endoparasites, excessive hair, or plant material).23 Eosinophilic IBD may also involve the stomach and/or colon.51 Diagnosis of EE is made via intestinal biopsy. Cats with primary lymphocytic-plasmacytic or lymphocytic IBD may also show subtle eosinophilic infiltrates on histopathology. In contrast, cats with EE have predominant tissue eosinophilia, variable mucosal architectural disturbances (eg, villus atrophy), and increased incidence of total intestinal wall thickening associated primarily with muscularis thickening as compared with cats with lymphocytic or lymphocytic-plasmacytic IBD.23,52 Diffuse disease is most common, but multisegmental EE has also been reported.52
No breed or sex predilections have been reported for EE in cats53,54; however, although cats of any age can be affected, the condition may be more common in mature cats (ie, 7-9 years). Clinical signs are similar to those of other forms of chronic gastroenteritis and may include vomiting, small- or large-bowel diarrhea, weight loss, and/or anorexia.53 Borborygmus, flatulence, abdominal pain, hematochezia, and mucoid stools are reported less commonly. Idiopathic EE may be solely or partially responsive to treatment with hypoallergenic diets and corticosteroids, which may be suggestive of an underlying immune disorder.52
Peripheral eosinophilia is not always present with EE but was observed in approximately 43% of cats in one study.52 If peripheral eosinophilia is associated with GI eosinophilic inflammation, other causes (eg, GI parasites, food-responsive enteropathy, intestinal neoplasia [eg, mast cell tumor, lymphoma], hypoadrenocorticism) should be ruled out.54 Parasitic infestation or dietary intolerance should be considered if moderate-to-large numbers of eosinophils are noted in intestinal biopsy samples with accompanying mild peripheral eosinophilia.53
Feline gastrointestinal eosinophilic sclerosing fibroplasia (FGESF) is a recently recognized nodular, nonneoplastic, densely fibroproliferative, eosinophil- and mast cell-rich inflammatory disease. It is thought to be a variant of EE.54-56 Its pathogenesis is unknown, but bacteria have been postulated to be an initiating factor due to their presence in 56% to 85% of cases55,57,58; however, antibiotic treatment alone is ineffective.55,57,58 Fungal infection has also been thought to be involved in the pathogenesis in some cases,59 but in other cases, no bacteria or fungi have been detected.55,56,60 Several other mechanisms (eg, penetrating wounds from a migrating foreign body, genetic eosinophil dysregulation, FHV-1, food hypersensitivity) have been proposed to be involved in the pathogenesis of FGESF.55,56 FGESF carries a guarded prognosis if untreated; however, survival times may be good in some cats, with some possibly surviving for years if they receive appropriate treatment, which includes a combination of surgery, antibiotics, and immunomodulatory drugs.57
Peripheral eosinophilia occurs more often in cats with FGESF than in cats with EE.52,55 One study reported that 58% of cats with FGESF had peripheral eosinophilia.55 If peripheral eosinophilia and an abdominal mass are observed, FGESF should be considered a differential diagnosis,57 although absence of peripheral eosinophilia alone does not rule out FGESF.57