This collection of diseases includes granulomatous enteritis (GE), lymphocytic-plasmacytic enterocolitis (LPE), multisystemic eosinophilic epitheliotropic disease (MEED), and idiopathic focal eosinophilic enterocolitis (IFEE). Disease is characterized by infiltration of the small and large intestine with inflammatory cells, including lymphocytes, plasma cells, macrophages, and eosinophils. The inflammatory condition may be limited to only a short segment of the bowel or be more diffuse. Malabsorption and a protein-losing enterocolopathy result. Diarrhea may or may not be a clinical feature. Inflammatory bowel disease should be considered in the differential diagnosis of horses with weight loss, recurrent colic, or hypoproteinemia, as well as in some horses with generalized skin disease.
Diagnosis is based on clinical signs, low serum protein concentration, possible thickened bowel (identified by ultrasonography or on rectal palpation), malabsorption, and intestinal or rectal biopsy. Malabsorption of carbohydrates occurs secondary to severe villous atrophy throughout the small intestine. Failure to absorb oral glucose or d-xylose verifies malabsorption from the small intestine.
Histologic diagnosis is subjective and should be performed by a pathologist experienced in reading equine intestinal biopsies. Rectal mucosal biopsy is useful in the diagnosis of ~50% of cases of GE and MEED but is rarely helpful in the diagnosis of LPE and IFEE. High numbers of eosinophils and lymphocytes can be identified in the intestinal wall of normal horses, but overinterpretation should be avoided. The presence of eosinophilic granulomas, vasculitis, and fibrinoid necrosis of intramural vessels is diagnostic of MEED. Horses with MEED may have severe dermatitis, eosinophilic infiltrations in the liver or pancreas, and sometimes marked eosinophilia. Horses with IFEE have eosinophilic infiltration restricted to the intestine and have a better prognosis for survival. Full-thickness intestinal biopsies can be obtained by using a laparoscopic procedure via a flank incision or by ventral midline celiotomy. Because most of the horses have severe hypoproteinemia at the time of diagnosis, incisional healing can be problematic.
The pathophysiology of the various syndromes is not well understood. An altered immune response to a common intestinal factor (eg, feed, parasites, bacteria) has been suggested. Histopathologic similarities exist between GE in horses, Johne's disease in cattle, and Crohn's disease in people. Standardbreds seemed to be predisposed to GE and MEED, which suggests possible genetic predisposition.
Various medical treatments have been tried with limited success. Corticosteroids, dietary alterations, metronidazole, and the antimetabolite azathioprine have been used. Hypereosinophilic syndrome in people often responds to hydroxyurea or vincristine, and sometimes interferon-α and cyclosporine are used. Supportive nutritional care should involve frequent feeding of good-quality, high-energy feeds. The prognosis is grave. If only a limited and accessible section of the bowel is affected, surgical removal may be successful. This is more common in IFEE, in which horses commonly present with colic rather than weight loss. Focal thickening, sometimes restricted to circumferential mural bands, is detected via exploratory laparotomy or necropsy; a diagnosis can be made by subsequent histopathology. Horses with IFEE respond to surgical resection of the diseased segment of intestine. Medical treatment with corticosteroids and feeding small frequent meals has also led to resolution of clinical signs after small-intestinal decompression without resection.