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Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
Rhinosporidiosis
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Rhinosporidiosis

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This slide presentation describes the unique disease entity rhinosporidiosis

This slide presentation describes the unique disease entity rhinosporidiosis

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  • 1. Rhinosporidiosis By Dr. T. Balasubramanian M.S. D.L.O.
  • 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. Rhinosporidium seeberi
    • Initially believed to be sporozoan
    • Classified under fungus - Olipidiaceae by Ashworth
    • Recently placed under DRIPS of aquatic protistan parasites
    • PCR tests have not demonstrated fungal proteins
  • 4. History
    • .
    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. Incidence / geographical description
    • .
    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. Theories of spread
    • .
    • Demellow's theory of direct transmission
    • Autoinoculation theory of Karunarathnae (responsible for satellite lesions)
    • Haematogenous spread - to distant sites
    • Lymphatic spread - causing lymphadenitis (rarity)
  • 7. Karunarathnae ‘s theory
    • .
    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. Reasons for endemicity
    • .
    • Physical characteristics of water in the ponds
    • Presence of synergistic aquatic organisms
    • Genetic predisposition in patients affected
    • Host immunity (lack of) or altered
  • 9. Life cycle (Ashworth)
    • .
    • Spore is the basic infecting unit.
    • It is about 7 microns in size
    • Also known as spherule
    • It has clear cytoplasm with 15 – 20 vacuoles filled with food matter
    • It is enclosed in a chitinous membrane
    • Found only in connective tissue spaces and is rarely intracellular
  • 10. Life cycle (Ashworth)
    • .
    • Spores start to increase in size
    • At 50 – 60 microns size granules start to appear. Nucleus prepares for cell division
    • Mitosis occur 4, 8, 16, 32 and 64 nuclei are formed
    • At 7th division size becomes 100 microns
    • Fully mature sporangium is 150 microns
    • Mature spores are found in the centre and immature ones at the periphery
  • 11. Life cycle (Ashworth)
    • .
  • 12. Life cycle (Recent)
    • .
    • Trophozoite (Juvenile sporangium) – 6 – 100 microns
    • It has single nucleus at 6 µ stage / Multiple nuclei at 100 µ stage
    • Lipid granules are seen in cytoplasm
  • 13. Life cycle (Recent)
    • .
    • Intermediate sporangium is 100 – 150 µ in diameter
    • It has bilamellar cell wall – outer chitinous and inner cellulose
    • Immature spores are seen within the cytoplasm
    • There are no mature spores seem inside the cytoplasm
  • 14. Life cycle (Recent)
    • .
    • Mature sporangium:
    • 100 – 400 microns
    • Cell wall is thin and bilamellar
    • Inside cytoplasm mature and immature spores are seen
    • These spores are embedded in mucoid matrix
    • Bilamellar cell wall has one weak spot – operculum
    • Spores mature in centrifugal and centripetal pattern
    • Mature spores are covered with mucoid material (comet of Beattee)
    • Mature spores give rise to electron dense granules which are the ultimate infecting unit
  • 15. Life cycle (Recent)
    • .
  • 16. Clinical classification
    • .
    • Nasal
    • Nasopharyngeal
    • Mixed
    • Bizzarre (ocular and genital)
    • Malignant rhinosporidiosis (cutaneous rhinosporidiosis)
  • 17. Common sites affected
    • .
    Nose - 78% Nasopharynx - 68% Tonsil - 3% Eye - 1% Skin - very rare
  • 18. Features of nasal Rhinosporidiosis
    • Lesions are polypoidal reddish and granular
    • Lesions may be multiple, pedunculated and friable
    • Surface is studded with whitish dots i.e. sporangia
    • The nasal lesions are highly vascular and bleeds on touch
    • The whole mass could be seen to be covered with mucous secretion
    • The lesion is restricted to nasal mucous membrane and does not cross the mucocutaneous junction
  • 19. Histopathology of nasal Rhinosporidiosis
    • Papillomatous hyperplasia of mucous membrane with rougae formation
    • Epithelium over sporangia is thinned out and giant cells could be seen in this area
    • Accumulation of mucous in the crypts
    • Increased vascularity due to angiogenesis factor
    • These spores stain with sudan black, Bromphenol blue
  • 20. Features of nasal Rhinosporidiosis
    • Chronicity
    • Recurrence
    • Dissemination
  • 21. Reasons of chronicity
    • Antigen sequestration
    • Antigenic variation
    • Immune suppression
    • Immune distraction
    • Immune deviation
    • Binding of host immunoglobulins
  • 22. Treatment
    • Surgery
    • Dapsone 100 mg /day – 6 months
  • 23.
    • .
    Thankyou

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