The taxonomy and phylogenetics of the human and animal pathogen Rhinosporidium seeberi: a critical review.

Rhinosporidum seeberi is the etiologic agent of rhinosporidiosis, a disease of mucous membranes and infrequent of the skin and other tissues of humans and animals. Because it resists culture, for more than 100 years true taxonomic identity of R. seeberi has been controversial. Three hypotheses in a long list of related views have been recently introduced: 1) a prokaryote cyanobacterium in the genus Microcystis is the etiologic agent of rhinosporidiosis, 2) R. seeberi is a eukaryote pathogen in the Mesomycetozoa and 3) R. seeberi is a fungus. The reviewed literature on the electron microscopic, the histopathological and more recently the data from several molecular studies strongly support the view that R. seeberi is a eukaryote pathogen, but not a fungus. The suggested morphological resemblance of R. seeberi with the genera Microcystis (bacteria), Synchytrium and Colletotrichum (fungi) by different teams is merely hypothetical and lacked the scientific rigor needed to validate the proposed systems. A fundamental aspect against the prokaryote theory is the presence of nuclei reported by numerous authors and updated in this review. Moreover, Microcystis's and Synchytrium's ultra-structural and key cell cycle traits cannot be found in R. seeberi parasitic phase. The PCR amplification of a cyanobacteria 16S rDNA sequence from cases of rhinosporidiosis, while intriguing, will be viewed here as an anomaly due to contamination with environmental Microcystis or perhaps as an endosymbiotic acquisition of plastids from cyanobacteria ancestors. Thus, even if R. seeberi possesses prokaryote DNA, this does not prove that R. seeberi is a cyanobacterium. The placement of R. seeberi within the fungi is scientifically untenable. The isolation and the DNA analysis performed in a fungal strain, and the lack of appropriate controls are the main problems of this claim. Further studies are needed to validate R. seeberi's acquisition of prokaryote plastids and other issues that still need careful scrutiny.

Recovery of growth of Hyphochytrium catenoides after exposure to environmental stress.

The survival of an isolate of Hyphochytrium catenoides collected from soil in the Blue Mountains in eastern New South Wales, Australia, was tested under extreme conditions in the laboratory. This isolate recovered growth after being subjected to drying on filter paper, to heat while desiccated, to hypersalinity, to strict anaerobic conditions, to freezing temperatures, and to a short period in solutions at pH 2.8-11.2. The capacity to survive under these conditions in the laboratory suggests adaptation to fluctuating conditions in the soil. The partial DNA sequence of the 28S ribosomal RNA gene in the isolate from New South Wales was 98% similar to that in an isolate from Arizona with a similar morphology.

Human anti-rhinosporidial antibody does not cause metabolic inactivation or morphological damage in endospores of Rhinosporidium seeberi, in vitro.

This report describes the use of the MTT-reduction and Evan's blue-staining tests for the assessment of the viability and morphological integrity, respectively, of rhinosporidial endospores after exposure to sera from rhinosporidial patients with high titres of anti-rhinosporidial antibody. Sera from three patients, with nasal, ocular and disseminated rhinosporidiosis respectively were used, with human serum without anti-rhinosporidial antibody for comparison, with or without added fresh guinea pig serum as a source of complement. All four sera tested, with or without guinea-pig serum, had no effect on the morphological integrity or the viability of the endospores and it is suggested that anti-rhinosporidial antibody has no direct protective role against the endospores, the infective stage, in rhinosporidiosis. This finding is compatible with the occurrence of chronicity, recurrence and dissemination that are characteristic of rhinosporidiosis despite the presence of high titres of anti-rhinosporidial antibody in patients with these clinical characteristics. The possible occurrence of humoral mechanisms of immunity that involve anti-rhinosporidial antibody with cells such as leucocytes and NK cells, in vivo, cannot yet be discounted, although the presence of high titres of anti-rhinosporidial antibody in patients with chronic, recurrent and disseminated lesions might indicate that such antibody is non-protective in vivo.

Rhinosporidiosis in Egypt: a case report and review of literature.

Rhinosporidiosis is an infection caused by Rhinosporidium seeberi that frequently presents as a polypoidal nasal lesions. Here, we report the first indigenous case of tumoral rhinosporidiosis in Egypt. In this case, a 25-year-old male patient from a rural background of Assuit City presented with epistaxis and a nasal polyp. The patient had not traveled abroad. The diagnosis was established on the morphological basis by the identification of 5- to 10-microm endospores and 50- to 1000-microm sporangia. The clinicopathological and immunologic features were discussed and the literature was reviewed. To the best of our knowledge this is the first case of this disease to be reported in Egypt in the human literature.

Anti-rhinosporidial antibody levels in patients with rhinosporidiosis and in asymptomatic persons, in Sri Lanka.

The only report hitherto, from India in 1982, on anti-rhinosporidial antibody levels in patients with rhinosporidiosis recorded that antibody was not detected in Indian patients. The present report describes the use of the dot-ELISA assay of serum anti-rhinosporidial IgG, IgM and IgA and salivary sIgA in patients with diverse clinical presentations, in rural asymptomatic persons who had bathed in ground waters that probably harboured the causative pathogen, Rhinosporidium seeberi, and in laboratory persons who were exposed to R. seeberi. Ultrasonic extracts of purified endospores and sporangia of R. seeberi were used as antigen. The geometric mean (reciprocal) titres of serum antibody detected in patients were IgM 142.1, IgG 178.5, IgA 84.6, with ranges of 0-640, 30-960 and 0-160 respectively, salivary sIgA titres ranged from 0 to 18 with a mean of 4.6. The levels of antibody had no correlation with the site, the number of sporangia, duration and recurrence of the disease. Asymptomatic persons from the same endemic area as patients showed mean titres of IgM 89.6, IgG 69.1, IgA 95.5, with salivary sIgA titres of 3.1. Asymptomatic personnel who had been working in a laboratory where rhiniosporidial work was being done, showed mean titres of 169.6 IgM, 62.8 IgG, and 6.5 salivary sIgA. These results indicate that an anti-rhinosporidial antibody response occurs in rhinosporidial patients, as well as in asymptomatic persons who were exposed to R. seeberi in the environment. Anti-R. seeberi antibody does not appear to be protective in rhinosporidiosis since appreciable titres were present in patients with recurrent, single, multiple or disseminated lesions of long duration.

Ocular rhinosporidiosis.

Rhinosporidium seeberi, the causative organism causing rhinosporidiosis, also affects extranasal sites. A 1 5-year-old male presented with a conjunctival fleshy swelling near the inner canthus of the left eye. His visual acuity was within normal range. Conjunctival papilloma was the provisional diagnosis for which he was operated on. Histopathology proved to be a case of ocular rhinosporidiosis. Six months follow-up of the case showed no recurrence.

Rhinosporidiosis--a clinicopathological study of 34 cases.

Rhinosporidiosis was the commonest (68%) fungal lesion encountered during the period of 11 1/2 years from January 1987 to July 1998. Men in 2nd, 3rd, 4th decade were commonly affected. Nose and nasopharynx were the commonest (85%) sites involved followed by ocular tissue (9%). One patient had involvement of bone (tibia). Generally a lymphoplasmacytic response was observed in all cases. Polymorphonuclear leukocytic response mostly observed at the site of rupture of sporangia. Epithelioid cell granulomatous and giant cell response observed in 47% of cases. Transepithelial migration of sporangia observed in 76% of cases. Rhinosporidium seeberi could be easily identified in haematoxylin and eosin stained sections. The walls of young trophic forms are delineated well with the PAS stain and verhoeff van Gieson stain.

Light and electron microscopic findings in rhinosporidiosis after dapsone therapy.

Morphological findings in serial nasal mucosal biopsies from three cases of rhinosporidiosis on dapsone therapy were compared with biopsies from 33 patients taken before dapsone or surgical treatment was initiated. All biopsies were examined by light microscopy and five by electron microscopy. Counts of histologically intact and degenerated organisms showed a decreasing proportion of intact forms with treatment.

Conjunctival oculosporidiosis in east Africa caused by Rhinosporidium seeberi.

BACKGROUND AND OBJECTIVE: Conjunctival rhinosporidiosis is an infectious disease rarely recorded outside the Indian subcontinent. The disease is caused by Rhinosporidium seeberi, an endosporulating microorganism of uncertain taxonomic classification. We report a series of cases manifesting this infection. MATERIAL AND METHODS: The demographic, clinical, and histopathologic data of 14 cases of conjunctival rhinosporidiosis on record at our Ophthalmic Pathology Laboratory were reviewed. RESULTS: All cases were from East Africa; 10 were from Malawi and 4 from Kenya. Ten specimens were from males and three from females. Their age ranged from 7 to 20 years. All patients were treated by surgical excision, and no recurrence was recorded. None of the cases was diagnosed clinically as rhinosporidiosis. Histologically, all stages of the organism's life cycle could be found in the excised tissue, from small trophocytes to large sporangia-containing sporoblasts. There were changes in histochemical stainings with growth and maturation. In general, the inflammation was of chronic nongranulomatous type. CONCLUSIONS: Conjunctival rhinosporidiosis is a rare infectious disease that typically appears in young males in rural regions, and that can be treated by surgical excision. It typically causes chronic nongranulomatous inflammation. Various stages of the R seeberi life cycle can be seen in the affected tissue.

Rhinosporidiosis: a description of an unprecedented outbreak in captive swans (Cygnus spp.) and a proposal for revision of the ontogenic nomenclature of Rhinosporidium seeberi.

Rhinosporidiosis is a mucocutaneous zooanthroponotic disease caused by Rhinosporidium seeberi, a fungal-like organism of uncertain classification with an unknown mode of transmission. Over a 3 year period, 41 captive swans (Cygnus olor and C. atratus) developed conjunctival and cutaneous polypoid lesions diagnosed as rhinosporidiosis by histopathological examination including light and electron microscopy. Investigation of this avian outbreak, the first of its kind, provides additional insight into the epidemiology of this enigmatic aetiologic agent, which has yet to be isolated and cultivated in vitro. The occurrence of rhinosporidiosis in swans supports an aquatic environment as the reservoir for R. seeberi, which is often associated with exposure to water. We report the first known occurrence of rhinosporidiosis in 41 captive mute (C. olor) and Australian black (C. atratus) swans dwelling on a lake in a Central Florida city. Additionally, we review the development stages of R. seeberi and propose a revision in its ontogenic nomenclature to reflect its probable taxonomic classification as a member of the kingdom Fungi.

Rhinosporidiosis.

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.

Cultivation of Rhinosporidium seeberi in vitro: interaction with epithelial cells.

Rhinosporidium seeberi, a fungus that is associated with polyp-like tumors in animals and man, was successfully cultivated. This organism stimulated proliferation of epithelial cells in vitro, producing polyp-like structures. Spores produced in culture required a period of aging or development, or both, before they were capable of reinitiating the growth cycle.

Rhinosporidiosis in Bahrain, Arabian Gulf.

Rhinosporidiosis occurred in Bahrain only in Indian expatriate workers who had the disease in India before coming to Bahrain. The pathological and clinical aspects of the disease as well as its possible health hazard in Bahrain are discussed.

Rhinosporidium seeberi: spherules and their significance.

This study of the nature and functional significance of the spherules that develop in sporoblasts show them to participate in the germination of Rhinosporidium seeberi and are the precursors of the trophocytes.

Rhinosporidium seeberi. An ultrastructural study of its endosporulation phase and trophocyte phase.

The endosporulation phase of Rhinosporidium seeberi is the part of the life cycle most vulnerable to drug therapy. The laminated body formed from the precleavage sporangium has double-membraned tubular and vesicular structures within concentric layers. Similar tubular structures are also found in the developing sporoblast. The development of trophocytes involves three distinct phases. The early trophocyte retains many of the characteristics of the sporoblast as well as endoplasmic reticulum and other radiating filamentous structures in the cell wall. The itermediate tropocyte is larger (20 mug to 30mug m) and contains lipid bodies and microbodies, whereas the mature trophocyte is smaller (7mug m to9mug m) and microbodies are sparse or absent.