Cluster of Nasal Rhinosporidiosis, Eastern Province, Rwanda.

We report 4 recent cases of nasal rhinosporidiosis in Rwanda. All patients were boys or young men living in the same district (Gatsibo District, Eastern Province), suggesting a reservoir in the area. The recent reemergence of rhinosporidiosis in Rwanda might reflect increased availability of diagnostic services rather than emerging disease.

Taxonomía y filogenética de Rhinosporidium seeberi, un patógeno para el ser humano y los animales: revisión crítica / The taxonomy and phylogenetics of the human and animal pathogen Rhinosporidium seeberi: a critical review

Rhinosporidum seeberi es el agente etiológico de la rinosporidiosis, una enfermedad de las membranas mucosas y, con menos frecuencia, de la piel y otros tejidos. Debido a que se resiste a crecer en los medios de cultivo desde hace más de 100 años, la identidad taxonómica de R. seeberi ha sido motivo de controversia. Tres nuevas hipótesis en una larga lista de puntos de vista similares han sido introducidas: 1) la cianobacteria Microcystis es el agente etiológico de la rinosporidiosis, 2) R. seeberi es un patógeno eucariota en los Mesomycetozoa, y 3) R. seeberi es un hongo. La literatura revisada sobre los estudios realizados con microscopia electrónica, los datos histopatológico y, más recientemente, los datos de varios estudios moleculares, apoyan fuertemente la idea de que R. seeberi es un patógeno eucariota, pero no un hongo. La semejanza morfológica propuesta por algunos de que R. seeberi es similar a los miembros de los géneros Microcystis (bacteria), Synchytrium y Colletotrichum (hongos) es meramente hipotética y no tiene el rigor científico necesario para validar el sistema propuesto. Un aspecto fundamental en contra de la teoría procariota es la presencia de núcleos descrita por numerosos autores y que actualizamos en esta revisión. Además, las características ultra-estructurales de los géneros Microcystis y Synchytrium y de sus ciclos celulares no han sido encontradas en la fase parasitaria de R. seeberi. La amplificación por PCR de una secuencia del rADN 16S típica de las cianobacterias en muestras de casos de rinosporidiosis, aunque interesante, será considerada en esta revisión como una anomalía debido a la contaminación con el medio ambiente (Microcystis) o tal vez como una adquisición endosimbiótica de plastidios a partir de cianobacterias ancestrales. Así pues, aunque R. seeberi podría poseer ADN procariota, esto no demuestra necesariamente que R. seeberi sea una cianobacteria. La clasificación de R. seeberi dentro de los hongos es insostenible. El aislamiento de un hongo, los análisis de ADN realizados, y la ausencia de controles apropiados son los problemas más importantes de esta teoría. Más estudios serán necesarios para validar la adquisición de plastidios procariotas en R. seeberi, y otros temas que requieren un cuidadoso escrutinio(AU)

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(AU)

Manifestaciones orales de patologías tropicales / Oral manifestations of tropical diseases

El presente trabajo expone las características clínias e histopatológicas de las pricnipales patologías tropicales (micóticas, parasitarias y virales) que presentan manifestaciones bucales, poniendo énfasis en la paracoccidioidomicosis, histoplasmosis, critpcocosis, dengue, leishmaniasis e infección micótica (AU)

Rinosporidiose: relato de um caso / Rhinosporidiosis: a case report

A rinosporidiose é uma doença inflamatória crônica, caracterizada por lesoes poliposas nas membranas mucosas, sendo causada pelo Rhinosporidium seeberi. É uma doença endêmica na India e Sri Lanka, e muito rara no Brasil e outros continentes. Apresentamos um caso em Vitória, ES, de um paciente proveniente do sul da Bahia que apresentava massa poliposa de cor avermelhada e granulosa, com aspecto de um morango na fossa nasal direita e que foi removida por microcirurgia transnasal. A massa tinha seu pedículo no septo nasal e após sua remoçao cauterizamos a base da lesao com eletro-cautério.

Rhinosporidiosis: three domestic cases.

Three cases of rhinosporidiosis in Americans who had not traveled abroad are reported. We believe this is the largest cluster of indigenous cases reported in the United States. The three patients had lived in rural northeast Georgia all of their lives. One had a polypoid conjunctival lesion, and the two others had nasal polyps. In each case, the diagnosis was made by demonstrating morphologically distinctive fungal elements in histopathologic sections. Clinically, rhinosporidiosis had not been suspected.

Unusual subcutaneous infections.

This article reviews various unusual subcutaneous infections, including rhinosporidiosis, lobomycosis, and protothecosis. Clinical findings, pathology, mycology, and treatment are discussed for each disease.

New interpretations in rhinosporidiosis, enigmatic disease of the last nine decades.

Fungal etiology is widely quoted for the disease rhinosporidiosis. Identity of the fungal sporangium and its relationship with the disease have baffled medical scientists and mycologists for several decades. This study provides unequivocal evidence against involvement of fungus in rhinosporidiosis. The so-called sporangium is found to be a unique body containing residue-loaded lysosomal bodies ('spores') for elimination from the system. 'Sporangia' have been redesignated nodular bodies (NB) and 'spores' as spheres of cellular waste (scw). Two carbohydrates, namely defective proteoglycans synthesized intracellularly and an exogenous polysaccharide ingested through diet of tapioca constitute indigestible material in NB and scw. Polysaccharide in NB which has beta, 1-4 glycosidic bonds between mannose residues is not degraded by gastrointestinal enzymes nor in intracellular lysosomes which break only alpha-glycosidic bonds. A link between NB and dry tapioca has been deduced. Rhinosporidiosis is a complex phenotype with perhaps no parallel in medical science. This report erases 99 years (1892-1991) of controversies regarding 'causal organism' of rhinosporidiosis.

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.