- Author: Duane R Hospenthal, MD, PhD, FACP, FIDSA, FASTMH; Chief Editor: Mark R Wallace, MD, FACP, FIDSA more...
Diagnosis is made by identifying the typical structures of R seeberi directly on microscopic examination. This includes examination of smears of macerated tissue or histology of prepared biopsy sample sections.
The organism can be observed with typical fungal stains (eg, Gomori methenamine silver [GMS], periodic acid-Schiff [PAS]), as well as with standard hematoxylin and eosin (H&E) staining.
Smears can also be observed with potassium chloride (KOH) preparation.
Serologic testing (immunoblot (dot – enzyme-linked immunosorbent assay [ELISA]) identification of antirhinosporidial antibody) has been developed and used for epidemiologic studies in endemic areas, but this testing is not available for or routinely used in patient diagnosis.[27, 26]
Recent evaluation of the use of computed tomography (CT) imaging to delineate the site and extent of disease has been published. Moderate-to-intense enhancement by CT was noted in the majority of lesions in the 16 people included in that study.
In 1923, Ashworth described in detail the life cycle of the organism in tissue. This cycle begins with a round endospore that is 6-10 µm in diameter. The endospore grows to become a thick-walled sporangium of 100-350 µm in diameter that contains up to several thousand endospores. These structures are similar to the smaller endospores (2-5 µm in diameter) and spherules (30-60 µm in diameter) of Coccidioides immitis.
The sporangia of R seeberi are observed under the normal epithelium. They are associated with immune cells, including neutrophils, lymphocytes, plasma cells, and multinucleated giant cells, often in scattered granuloma. Papillomatous hyperplasia and hypervascularity are also common. See the images below.
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