Linton M, Nimmo JS, et al. Feline gastrointestinal eosinophilic sclerosing fibroplasia: 13 cases and review of an emerging clinical entity. J Feline Med Surg 2015; 17(5):392-404.
Middle-aged to older cats presenting with signs of chronic gastrointestinal disease: vomiting, diarrhea, weight loss, and an appetite history that may vary from polyphagia to anorexia, are seen daily in primary clinical practice. On palpation of the abdomen, single or multiple mass effects, diffuse or segmental thickening of the intestines, intra-abdominal lymphadenopathy, or no abnormalities at all may be identified. Further diagnostic evaluation of the patient often identifies inflammatory or neoplastic gastroenteritidies such as inflammatory bowel disease or lymphoma as the etiology.
A recently identified inflammatory disease of felines affecting stomach or intestines is feline gastrointestinal sclerosing fibroplasia (FGESF), which has been found in cats in the USA, Europe, Japan, Australia, and New Zealand. In this study of 13 cases of FGESF, all patients were neutered, and most were male (9/13). The cats were middle-aged for the most part (median age, 7 years; range 2-11 years); 7 were Ragdolls, 5 were domestic shorthairs, and one was a Persian. The dietary history of the subjects was varied, but typically included commercial canned and dry food; no cats had been fed raw meat bones on a regular basis. Chronic vomiting and/or diarrhea for a minimum of 3 months and often for more than 12 months was reported in 91% of the patients; 77% had weight loss, 62% lethargy, and anorexia was noted in 46%. One animal presented in respiratory distress and had a pleural effusion. Only one of the cats had no reported clinical signs. A firm, irregular, fixed abdominal mass in the cranial and/or mid-abdomen was identified in 11/13 (85%) of the patients. The two cats in whom an abdominal mass was not palpated were lethargic, anorexic, and had a history of vomiting. None of the patients had a previous history of foreign body or hairball intestinal obstruction.
Clinicopathologic evaluation of the cats also demonstrated significant abnormalities. Hyperproteinemia of hyperglobulinemia was present in 7/11 cats. Some patients (5/11) were hypoalbuminemic. Five out of 10 cats had a peripheral eosinophilia. Two of the cats had a mild non-regenerative anemia. Retrovirus testing was conducted on only two animals, both of whom were seronegative for feline leukemia virus antigen as well as feline immunodeficiency virus antibody.
Full thickness gastrointestinal biopsies and/or incisional biopsies of mesenteric lymph nodes were performed in all 13 patients. FGESF was diagnosed on finding the presence of eosinophilic inflammation with fibroplasia, including broad mature collagen bundles in multiple sections. Lesions of FGESF have a coarse, gritty feel, which originates from the abundance of collagen trabeculae they contain. These lesions were found at the ileocecocolic junction in 8 cats, at the pylorus in 2 cats, and on the greater curvature of the stomach in one. In all cases, the histological diagnosis of FGESF determined by the original pathologist was confirmed by a second pathologist.
A number of special stains were used to determine whether or not infectious agents such as bacteria, protozoa, or fungi were present in the biopsies. Tissue samples were cultured for bacteria in 3 of the cases. Immunohistochemistry for feline coronavirus and feline herpesvirus type 1 was also performed on the biopsies, and was negative in 12/12 cats tested. Further investigation of the samples for bacterial DNA was done utilizing fluorescence in situ hybridization. In 10/13 patients, mesenteric lymphadenomegaly was found, and these lymph nodes demonstrated lymphoid hyperplasia and eosinophilia. In biopsies of 8/13 cats, bacteria were identified on histology; bacteria identified using the various diagnostic tests employed in the study included Clostridium sp., E. coli, and Providencia stuartii. In 2 of the 8 cats in which bacteria were detected histologically, none were detected using DNA probes. The presence of bacteria in many of the lesions does not necessarily have an etiological relationship with the disease; the lesions were often ulcerated and communicated with the lumen of the gastrointestinal tract.
The etiopathogenesis of FGESF is unknown, but suspected to be due to immunological dysregulation associated with adverse reactions to food, dysbiosis of the gut microbiota, ingestion of ectoparasites, endoparasites (in pumas, FGESF-like lesions may be associated with the presence of nematodes) such as ascarids, or excessive ingested hair (the majority of patients in this study were longhairs) or plant material.
Prognosis for cats with FGESF appears guarded at best, although some of the poor outcomes may have been due to late diagnosis and suboptimal management. With early and appropriate treatment, the authors state that survival times can actually be good. Eight of the 13 cats died or were euthanized; 3 of these died perioperatively; mean survival time for these 8 cats was 2-152 days. Of the 5 surviving cats, survival time after diagnosis ranged from 1-10 years.
For the clinician presented with a cat having a palpable abdominal mass and a history of vomiting, diarrhea, lethargy, and/or anorexia, FGESF should be considered. It is potentially easy to confuse the mass lesions of FGESF with lymphoma, adenocarcinoma, or granuloma, and the hard, gritty feel of FGESF lesions on aspiration, biopsy, or excision may help differentiate FGESF from these other diseases. Although diagnostic imaging and needle aspiration may be useful in developing a provisional diagnosis of FGESF, in most cases laparotomy and biopsy/histopathology (including special stains) will be necessary for definitive diagnosis and development of therapy. Multimodal therapy, involving immunomodulatory drugs such as prednisolone, chlorambucil, cyclosporine, hydroxyurea, and/or lomustine; antibiotic therapy, such as a combination of amoxicillin-clavulanate and metronidazole, or marbofloxacin and metronidazole; and cytoreduction via surgical debulking, is likely to be associated with the best patient outcomes and is recommended by the authors. Surviving patients who were monitored with blood panels demonstrated resolution of both hyperglobulinemia and eosinophilia following therapy. Finally, owners must be educated regarding chronic vomiting in their cats; this clinical sign should not be trivialized or ignored and considered “normal” for felines, but should trigger prompt evaluation by a veterinarian. [PJS]
Craig LE, Hardam EE, et al. Feline gastrointestinal eosinophilic sclerosing fibroplasia. Vet Pathol 2009;46:63-70.
Weissman A, Penninck D, et a. Ultrasonographic and clinicopathologic features of feline gastrointestinal eosinophilic sclerosing fibroplasia in four cats. J Feline Med Surg 2013;15:148-54.