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A morphological study on equine granulomatous enteritis (EGE) in 13 horses is presented. All horses were young (1 to 5 years old) standardbreds. Based on gross pathology, cases were classified into those with diffuse (11 cases) and those with localized (2 cases) small bowel lesions. The granulomatous reaction in the gut was marked by diffuse and patchy infiltrates and distinct granulomas, composed of epithelioid cells, macrophages and lymphoid cells, and was devoid of necrosis. Salient accompanying features of the small bowel included lymphoid hyperplasia, peri-lymphatic and transmural inflammation, lymphangiectasia, villous atrophy, mucosal ulcerations and crypt abscesses. Granulomatous changes were often demonstrated in alimentary tract tissues beyond the small bowel and its lymph nodes and were in some cases shown to occur multi-systemically. The morphology and epidemiological features of the condition suggest a specific aetiology. The histology indicated that an immune reaction was operative and that inflammation of the lamina propria was an early event in the pathogenesis of the gut lesion. No conclusive evidence of a specific infectious cause was found. It is suggested that the disease might be associated with intrinsic disturbances of inflammatory defence mechanisms.

The jejunal mucosa of 4 cases of equine granulomatous enteritis and 2 control horses was investigated by light microscopy and by scanning and transmission electron microscopy. Attention was focused upon changes in mucosal topography and enterocyte morphology in the inflamed mucosa. Structural changes ranged in severity from only a slight thickening and shortening of villi to the appearance of a virtually flat mucosa, upon which crypts opened directly or through shallow cavities encircled by collars of epithelial cells. Between these extremes, the mucosa showed a variety of patterns, all characterized by distinctly abnormal villus projections. These were often united by epithelial bridges and were commonly markedly short, broad and irregular. Enterocytes of mildly changed mucosae showed a normal histology and fine structure, whereas more severely changed specimens displayed a flattened surface epithelium with ultrastructural abnormalities, the most consistent being a pronounced shortening of microvilli. In particular, greatly flattened cells showed evidence of cellular injury, such as prominence of cytolysosomes and degenerative changes of the rough endoplasmic reticulum, while other cells were chiefly characterized by an abundance of non-membrane-bound ribosomes and other features signifying an immature state. Cell-membrane-tight junctions of the surface epithelium appeared to be intact. No intracellular micro-organisms were detected. It is suggested that several factors are involved in the creation of the abnormal mucosal topography in this disease, including excessive enterocyte loss, crypt cell destruction, inflammatory distension of villi and villus fusions.

Clinical and pathological features of a variety of forms of feline colitis or enterocolitis were examined and classified into 9 separate entities: Salmonella enterocolitis, the colitis of feline infectious peritonitis, mycotic enterocolitis, acute angiopathic colitis, acute angiopathic colitis with ischaemic ulcers, feline granulomatous colitis, the colitis of feline panleucopenia, feline histiocytic colitis, and feline ulcerative, lymphocytic mucosal-submucosal colitis.

Widespread cutaneous papules in a yearling Standardbred filly were attributed by light and electron microscopic examination to molluscum contagiosum. Concomitant granulomatous enteritis, suspected clinically due to protein-losing enteropathy, was verified histopathologically. An associated altered altered immune response is suggested as the reason for the widespread poxvirus infection.