Rhinosporidiosis.

Abstract

Rhinosporidium seeberi, the causative organism of rhinosporidiosis of the nasal mucosa and skin was reviewed with regard to its pathogenesis and histopathology, histochemistry, ultrastructure, life cycle, and cultivation. The pathological findings from infected tissues reveal a granulomatous reaction comprising mixed cell granuloma, pseudocystic abscesses, fibrosis around the causative organism (R. seeberi), and transepidermal elimination. The cell walls of trophocytes and sporangia exhibit the presence of cellulose. The spore wall is encapsulated with granular fibrillary substances consisting of acid mucopolysaccharides. Spheroid bodies have proved to be DNA surrounded by a thin membrane-bound layer. In the cytoplasm of the organism, various substances can be detected by histochemical methods (e.g., glycogen, glycoprotein, acid mucopolysaccharides, neutral lipids, and phospholipids). The walls of the sporangia are found to be trilaminated, whereas those of trophocytes are bilaminated. There is a myriad of curvilinear structures around the outer wall of both forms. The ultrastructure of a trophocyte shows it to be comprised of sporoblasts containing oval or round membrane-bound nuclei with nucleoli, mitochondria, endoplasmic reticulum, chromatin granules, vacuoles, lipid bodies, and spherules. We suggest that the multilamellar bodies are precursors of trophocytes and sporangia. Abortive trophocytes without cytoplasmic organelles are seen, and they collapse at the end of the maturation process. Rhinosporidium seeberi fails to grow in any of the artificial media used but can be maintained through its life cycle in tissue cultures.