Basophilic background with abundant fine eosinophilic rod-shaped granules and free bacterial organisms, high cellularity. The sample consisted of a prevalent mixed population of eosinophils and degenerated neutrophils, occasionally  engulphing bacteria, mostly thin and short rods. A consistent population of plump spindle cells, individualized or arranged in loosely or tightly cohesive groups was observed; cytoplasm was basophilic, moderate in amount, with distinct or irregular margins, occasionally elongated in tails. Nuclei were round to oval, paracentric,  from 2 to 5 RBCs in diameter, with finely stippled chromatin and 1-3 large prominent nucleoli.  Additionally, several foamy macrophages engulphing cellular debris, occasional individualized well-differentiated mast cells, rare small and medium-sized lymphocytes and plasma cells were noted.

Septic mixed inflammation, primarily eosinophilic and neutrophilic associated with atypical mesenchymal cell; this picture indicates FGEFS  as the primary diagnosis. Culture with sensitivity is recommended; histopathology is necessary to confirm the cytological diagnosis.

Feline Gastrointestinal eosinophilic sclerosing fibroplasia (FGESF) in cats is a  recently described inflammatory non-neoplastic disease that presents as eosinophilic mass(es) in  the gastrointestinal tract and associated abdominal lymph nodes. This condition is most commonly seen in middle aged and male cats of all breeds, with Ragdolls being overrepresented, suggesting a possible breed predisposition. The disease can affect cats of  any age (1–16 years old), although is mostly diagnosed in adult cats aged 7–8 years. The most common presenting signs of cats with GESF are chronic vomiting, diarrhea, followed by weight loss, lethargy, and, on other occasions, constipation, as intestinal fibrosis causes stenosis and signs of obstruction.   A palpable intestinal mass is reported in 85% to 100% of cases; mass are localized  mainly in the stomach, pyloric sphincter,  ileum, ileocecocolic junction, and colon. The mesenteric lymph nodes may also be affected, with subsequent mesenteric lymphadenomegaly.  Extraintestinal localizations have uncommonly been reported and include  mesentery, retroperitoneum, medial retropharyngeal lymph node and cranial mediastinum.

Eosinophilic inflammation is considered a key feature in this disease, however etiopathogenesis remains poorly understood. Several hypothesis have been proposed and include:

• Presence of an immunologic dysregulation triggered by one of multiple possible causes (parasitism, food allergy, dysbiosis, IBD, inherited genetic mutation leading to eosinophil dysregulation)
• Presence of different microorganisms such as bacteria, fungi or protozoan (toxoplasma) has been associated with lesions; however, antibiotic therapy is not effective in treating the condition and no infectious etiology was reported in nearly half of cases in one report
• A genetic predisposition has been hypothesized, whereby some cats (e.g. Ragdolls cat) may develop eosinophilic inflammation in response to certain antigens in the intestinal environment

In general, sclerosing fibrosis is thought to be driven by the stimulation of fibrogenic mediators produced by activated eosinophils, such as transforming growth factor (TGF-β) and interleukin-1 (IL-1). These mediators can lead to fibroblast proliferation and the deposition of extracellular matrix proteins. Some Authors consider FGESF another manifestation of species-specific unique exuberant inflammatory response to chronic bacterial infections and other infectious entities; the histologic commonalities and the response to immunomodulatory therapy for eosinophilic sclerosing fibroplasia/lymphadenitis and other eosinophilic inflammatory diseases in cats support this  hypothesis.

the most common reported abnormalities are  eosinophilia mostly moderate to severe,  which is present in about half of the cases. Other  less common clinicopathological abnormalities are  anemia,  neutrophilia, monocytosis, lymphocytosis, hypoalbuminemia, hyperglobulinemia, hypocholesterolemia, total hypocalcemia.

Ultrasonography in  association with cytological examination is useful to focus the diagnosis of FGESF, although  the definitive diagnosis is made through histopathology. FGESF should be considered  when abdominal ultrasonographic findings reveal typical features such as a loss of intestinal layering, muscularis layer thickening, and mixed wall echogenicity with hyperechoic areas.  Cytological examination is frequently unrewarding, showing eosinophilic inflammation, mixed inflammation or necrosis; fibroblasts are often absent in cytological samples, likely due to their low tendency to exfoliate. Other inflammatory cells including small lymphocytes and mast cells may be present, as well as bright pink ribbons of collagen. Bacterial sepsis is common and intralesional fungal organisms have rarely been reported also. Characteristic histopathologic findings include dense branching collagen trabeculae, interspersed by large reactive fibroblasts, and mixed inflammatory cell infiltrates, predominately eosinophils.  The main cytological and histological differential diagnoses to consider are mast cell tumor, sarcoma, and T-cell lymphoma. A case series  documented intestinal sclerosing mast cell neoplasm in cats, which were accompanied by eosinophilic infiltrates, but it is currently controversial whether these are true neoplasms or a variant of FGESF.  Recently, a form of  FGESF  with intralesional lymphoma has been described, for which the term eosinophilic sclerosing lymphoma is proposed. Histologic and  immunohistochemical characterization of this unique lymphoma revealed that the neoplastic lymphocytes were immunopositive for CD56 and/ or CD3, suggesting a natural killer cell, natural killer T-cell, or T-cell origin.

The prognosis for cats with GESF is reported as variable, varying  from guarded, to cats living for several years. Surgical removal of the mass has been performed in most cases; however, several studies report medical management with administration of corticosteroids, cyclosporine, and mycophenolate. Cats being treated with surgery alone have a significantly shorter  survival time than those cats treated with surgery and corticosteroids. Most cats surviving the perioperative period remained well for several years. A mass in a second location can develop in some of  the cases, after surgical removal of the initial mass.

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Schulman EY,  Lipscomb TP. Letters to the editor and rebuttal regarding the paper recently published in Veterinary and Comparative Oncology, “feline intestinal sclerosing mast cell tumour: 50 cases (1997-2008) 2010;8:72-79”  by C. H. C. Halsey, B. E. Powers and D. A. Kamstock. Letter to the editor #1. Vet Comp Oncol. 2010;8:235–236; author reply 236-242.

Linton M, Nimmo JS, Norris JM, et al. Feline gastrointestinal eosinophilic sclerosing fibroplasia: 13 cases and review of an emerging clinical entity. J Feline Med Surg. 2015;17:392–404.

Porras N, Rebollada Merino-A, Rodriguez-Franco F, et al. Feline gastrointestinal eosinophilic sclerosing fibroplasia–extracellular matrix proteins and TGFß1 immunoexpression. Vet Sci. 2022;9(6):291.

Zampieri B, Church ME, Walsh K, et al. Feline eosinophilic sclerosing fibroplasia-a characteristic inflammatory response in sites beyond the gastrointestinal tract: case report and proposed nomenclature. JFMS Open Rep. 2022;8(2):1–6