Feline gastrointestinal eosinophilic sclerosing fibroplasia in two cats

Siobhan O’Sullivan

Animal Health Laboratory, University of Guelph, Guelph, ON

AHL Newsletter 2021;25(4):25.

Duodenal lesions were identified in two domestic short-haired cats consisting of incidental mural thickening and ulceration in a 6-month-old cat presenting for workup of post-anesthetic mortality, and an intramural mass in a 3-year-old cat exhibiting gastrointestinal symptoms.  Examination of the duodenum in both cats revealed a similar histologic lesion.  Expanding the intestinal wall were anastomosing trabeculae of eosinophilic matrix (collagen) interspersed with streams of plump spindle cells (reactive fibroblasts) and eosinophils, compatible with feline gastrointestinal eosinophilic sclerosing fibroplasia (FGESF) (Figs. 1, 2).

There have been approximately five cases of FGESF submitted to the AHL from 2015-2021.  Cats tend to present clinically with gastrointestinal symptoms (vomiting, weight loss) and may have a palpable abdominal mass.  Cats of various ages are reportedly affected, ranging from 14 weeks-16 years, although middle-aged cats are overrepresented.  Relevant and relatively consistent clinical findings include: peripheral eosinophilia; a notably ‘gritty’ resistance to fine needle aspiration due to the collagen content of the mass; and aspirate cytology dominated by eosinophils.  Gross lesions are described as focal raised firm masses that can expand to obstruct the lumen, most often located near the pylorus or ileocecocolic junction, but appearing anywhere along the gastrointestinal tract.  Histologic lesions can also appear in adjacent lymph nodes.

The underlying cause of FGESF is currently unknown.  Prior to emerging as a distinct entity, differential diagnoses for FGESF included fibrosarcoma, extra-skeletal osteosarcoma or a sclerosing variant of gastrointestinal mast cell tumor.  Various bacteria have been detected within FGESF masses by culture or fluorescence in situ hybridisation (FISH).  Zygomycetes and nematodes have been less frequently associated with FGESF.  However, no infectious agent has been consistently implicated, and ulcerated FGESF masses are often considered secondarily infected by normal intestinal flora.  A mechanical component to the pathogenesis has been suggested, with trauma from foreign bodies or ingested hair at sites of gastrointestinal narrowing (pylorus, ileocecocolic junction), allowing for bacterial invasion and subsequent inflammation.  FGESF lesions may represent an immune-mediated, self-perpetuating eosinophilic inflammatory response following exposure to unknown antigens, with a genetic predisposition for a dysregulated immune response being the primary contributor.  The significance of any breed predisposition or hereditary component is currently undescribed.  It has also been suggested that FGESF may represent another aspect of the feline eosinophilic granuloma complex known to produce oral and cutaneous lesions.

Given the few reported cases of FGESF, the prognosis is not well known, but is considered guarded.  With complete excision, immunosuppression and antibiotic therapy, many cats see resolution of the clinical signs without evidence of recurrence, but there are reported exceptions.   AHL

Figure 1. Expanding the duodenal wall are anastomosing trabeculae of deeply eosinophilic collagen (arrows).  H&E.

Figure 2. Reactive fibroblasts and eosinophils (thick arrows) surround the collagen trabeculae (thin arrow).  H&E.

References

1. Craig L, et al. Feline gastrointestinal eosinophilic sclerosing fibroplasia. Vet Pathol 2009;46:63–70.

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