Culture of the organism that causes rhinosporidiosis.

The causative agent of rhinosporidiosis is a microscopic round body in polypoidal masses that is believed to be the sporangium of a fungus Rhinosporidium seeberi. But fungal aetiology can not be proved with certainty. Attempts to culture the fungus on various media have also been unsuccessful. In a recent study pond water samples, from water in which patients had been bathing, were analysed and a unicellular prokaryotic cyanobacterium Microcystis aeruginosa was isolated. The same cyanobacterium was demonstrated in clinical samples from patients with rhinosporidiosis. Consequent to these findings, attempts were made to culture the causative organism of rhinosporidiosis under conditions that support growth of cyanobacteria. This study describes a simple method for laboratory culture of this organism. Observations based on laser-scanning confocal microscopy, light and electron microscopy confirm that a cyanobacterium, Microcystis sp. is the causative agent of the disease. Rhinosporidiosis is the first human disease to be shown to be caused by a cyanobacterium. The findings have opened the way for development of therapy.

Rhinosporidiosis: a study that resolves etiologic controversies.

We have been able to isolate the cyanobacterium Microcystis aeruginosa from water samples of ponds and river where patients of rhinosporidiosis were bathing. It is likely that this cyanobacterium is the causative agents of this disease. The bluish-green cells of M. aeruginosa also have a colorless small cell stage called nanocyte which has been detected in clear waters of all the pond and river samples studied. Both large cells and nanocytes of M. aeruginosa could be recognized inside the round bodies of rhinosporidiosis by light and electron microscopy. Further work on culturing this organism from excised samples and evaluation for drug therapy are in progress. It is hoped that, if therapy becomes available, no surgery would be required for this disease. It is suggested that the waters from ponds and lakes, as well as municipal and recreational waters, be checked for the nanocyte stage of M. aeruginosa. Etiological controversies of rhinosporidiosis have been reasonably solved. The new findings justify a change in the name "rhinosporidiosis" that had been associated with the fungus Rhinosporidium Seeberi.

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 associated with squamous cell carcinoma in the tongue.

The peritumoural region of a squamous cell carcinoma of the tongue when examined with light and electron microscope showed nodular bodies in the submucosa with all the distinctive features of 'sporangium and 'spores' of rhinosporidiosis. The occurrence of rhinosporidiosis in the tongue along with malignancy has not been reported hitherto. Some interesting observations and causal relationships are discussed.

Ultrastructural features that relate to tumor cell behaviour in human breast carcinomas.

Human breast tumor biopsies were studied by transmission electron microscopy for ultrastructural characteristics that might be associated with tumor cell function and behaviour. Features related to the state of cell differentiation and tumor cell detachment were evaluated and discussed. The ultrastructure of loose cells at the tumor periphery is compared with that of coherent cells in interior regions. Structural information has been analysed by taking into account available biochemical data for interpretation of cell function. The value of the parameters chosen for study is discussed. This study shows that each tumor needs to be evaluated independently for its specific ultrastructural features. Electron microscopic data becomes more relevant when interpreted in conjunction with histological diagnosis and clinical findings.

Comparative ultrastructure of cancerous and normal human breast cells: demonstration of cytoskeleton by TEM.

A technique for the study of the cytoskeleton by transmission electron microscopy is described. It preserves cytoplasmic and nuclear ultrastructural details as well as cytoskeletal elements enabling a correlated study. There are no significant differences in organization and distribution of intermediate filaments between cancerous and normal breast cells. Close association between cytokeratin filaments and cell structures has been established from stereotilted images. Cytokeratin filaments in contact with cell structures are in the form of bundles; in the free 'space' of cytoplasm meshworks are organized. The intermediate filament system could possibly be organized for participation in diverse functions in a cell.