Rhinosporidiosis

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This slide presentation describes the unique disease entity rhinosporidiosis

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Rhinosporidiosis

  1. 1. Rhinosporidiosis By Dr. T. Balasubramanian M.S. D.L.O.
  2. 2. Definition Rhinosporidiosis has been defined as a chronic granulomatous disease characterized by production of polyps and other manifestations of hyperplasia of nasal mucosa. The etiological agent is Rhinosporidium seeberi.
  3. 3. Rhinosporidium seeberi <ul><li>Initially believed to be sporozoan </li></ul><ul><li>Classified under fungus - Olipidiaceae by Ashworth </li></ul><ul><li>Recently placed under DRIPS of aquatic protistan parasites </li></ul><ul><li>PCR tests have not demonstrated fungal proteins </li></ul>
  4. 4. History <ul><li>. </li></ul>1892 - Malbran observed the organism in nasal polyp 1900 - Seeber described the organism 1903 - O'Kineley described its histology 1905 - Minchin & Fantham studied O'Kineley's tissue and named the organism as Rhinosporidium Kinealyi 1913 - ZSchokke reported similar organism in horses and named it Rhinosporidium equi 1923 - Ashworth described its life cycle 1924 - Forsyth described skin lesion 1924 - Thirumoorthy reported the first female patient 1936 - Cefferi establised the identity of R. Seeberi and R. Equi 1953 - Demellow described the mode of its transmission
  5. 5. Incidence / geographical description <ul><li>. </li></ul>More than 90% of cases have been reported from India / Srilanka Madurai, Ramnad, Rajapalayam, and Sivaganga are endemic zones in Tamilnadu Transmission is possibly due to taking bath in common ponds
  6. 6. Theories of spread <ul><li>. </li></ul><ul><li>Demellow's theory of direct transmission </li></ul><ul><li>Autoinoculation theory of Karunarathnae (responsible for satellite lesions) </li></ul><ul><li>Haematogenous spread - to distant sites </li></ul><ul><li>Lymphatic spread - causing lymphadenitis (rarity) </li></ul>
  7. 7. Karunarathnae ‘s theory <ul><li>. </li></ul>Karunarathnae postulated that Rhinosporidium seeberi existed in a dimorphic state. It existed in a saprophytic form in soil and water. It took a yeast form inside tissues. This ability to exist in dimorphic state helps it to survive hostile environment for a long period of time.
  8. 8. Reasons for endemicity <ul><li>. </li></ul><ul><li>Physical characteristics of water in the ponds </li></ul><ul><li>Presence of synergistic aquatic organisms </li></ul><ul><li>Genetic predisposition in patients affected </li></ul><ul><li>Host immunity (lack of) or altered </li></ul>
  9. 9. Life cycle (Ashworth) <ul><li>. </li></ul><ul><li>Spore is the basic infecting unit. </li></ul><ul><li>It is about 7 microns in size </li></ul><ul><li>Also known as spherule </li></ul><ul><li>It has clear cytoplasm with 15 – 20 vacuoles filled with food matter </li></ul><ul><li>It is enclosed in a chitinous membrane </li></ul><ul><li>Found only in connective tissue spaces and is rarely intracellular </li></ul>
  10. 10. Life cycle (Ashworth) <ul><li>. </li></ul><ul><li>Spores start to increase in size </li></ul><ul><li>At 50 – 60 microns size granules start to appear. Nucleus prepares for cell division </li></ul><ul><li>Mitosis occur 4, 8, 16, 32 and 64 nuclei are formed </li></ul><ul><li>At 7th division size becomes 100 microns </li></ul><ul><li>Fully mature sporangium is 150 microns </li></ul><ul><li>Mature spores are found in the centre and immature ones at the periphery </li></ul>
  11. 11. Life cycle (Ashworth) <ul><li>. </li></ul>
  12. 12. Life cycle (Recent) <ul><li>. </li></ul><ul><li>Trophozoite (Juvenile sporangium) – 6 – 100 microns </li></ul><ul><li>It has single nucleus at 6 µ stage / Multiple nuclei at 100 µ stage </li></ul><ul><li>Lipid granules are seen in cytoplasm </li></ul>
  13. 13. Life cycle (Recent) <ul><li>. </li></ul><ul><li>Intermediate sporangium is 100 – 150 µ in diameter </li></ul><ul><li>It has bilamellar cell wall – outer chitinous and inner cellulose </li></ul><ul><li>Immature spores are seen within the cytoplasm </li></ul><ul><li>There are no mature spores seem inside the cytoplasm </li></ul>
  14. 14. Life cycle (Recent) <ul><li>. </li></ul><ul><li>Mature sporangium: </li></ul><ul><li>100 – 400 microns </li></ul><ul><li>Cell wall is thin and bilamellar </li></ul><ul><li>Inside cytoplasm mature and immature spores are seen </li></ul><ul><li>These spores are embedded in mucoid matrix </li></ul><ul><li>Bilamellar cell wall has one weak spot – operculum </li></ul><ul><li>Spores mature in centrifugal and centripetal pattern </li></ul><ul><li>Mature spores are covered with mucoid material (comet of Beattee) </li></ul><ul><li>Mature spores give rise to electron dense granules which are the ultimate infecting unit </li></ul>
  15. 15. Life cycle (Recent) <ul><li>. </li></ul>
  16. 16. Clinical classification <ul><li>. </li></ul><ul><li>Nasal </li></ul><ul><li>Nasopharyngeal </li></ul><ul><li>Mixed </li></ul><ul><li>Bizzarre (ocular and genital) </li></ul><ul><li>Malignant rhinosporidiosis (cutaneous rhinosporidiosis) </li></ul>
  17. 17. Common sites affected <ul><li>. </li></ul>Nose - 78% Nasopharynx - 68% Tonsil - 3% Eye - 1% Skin - very rare
  18. 18. Features of nasal Rhinosporidiosis <ul><li>Lesions are polypoidal reddish and granular </li></ul><ul><li>Lesions may be multiple, pedunculated and friable </li></ul><ul><li>Surface is studded with whitish dots i.e. sporangia </li></ul><ul><li>The nasal lesions are highly vascular and bleeds on touch </li></ul><ul><li>The whole mass could be seen to be covered with mucous secretion </li></ul><ul><li>The lesion is restricted to nasal mucous membrane and does not cross the mucocutaneous junction </li></ul>
  19. 19. Histopathology of nasal Rhinosporidiosis <ul><li>Papillomatous hyperplasia of mucous membrane with rougae formation </li></ul><ul><li>Epithelium over sporangia is thinned out and giant cells could be seen in this area </li></ul><ul><li>Accumulation of mucous in the crypts </li></ul><ul><li>Increased vascularity due to angiogenesis factor </li></ul><ul><li>These spores stain with sudan black, Bromphenol blue </li></ul>
  20. 20. Features of nasal Rhinosporidiosis <ul><li>Chronicity </li></ul><ul><li>Recurrence </li></ul><ul><li>Dissemination </li></ul>
  21. 21. Reasons of chronicity <ul><li>Antigen sequestration </li></ul><ul><li>Antigenic variation </li></ul><ul><li>Immune suppression </li></ul><ul><li>Immune distraction </li></ul><ul><li>Immune deviation </li></ul><ul><li>Binding of host immunoglobulins </li></ul>
  22. 22. Treatment <ul><li>Surgery </li></ul><ul><li>Dapsone 100 mg /day – 6 months </li></ul>
  23. 23. <ul><li>. </li></ul>Thankyou

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