RHINOSPORIDIOSIS.pptx

Rhinosporidiosis

1. RHINOSPORIDIOSIS

2. RHINOSPORIDIOSIS It is a chronic granulomatous disease caused by Rhinosporidium seeberi Disease is also seen to involve animals such as cows, bulls,horses, mules and dogs where men and animals share the same infected ponds In India, disease is more common in the southern states. It is prevalent in the states of Tamil Nadu, Kerala,Madhya Pradesh, Chhattisgarh, Puducherry and Andhra Pradesh

3. AETIOLOGIC AGENT It has been difficult to classify this organism. It has not been cultured so far. Initially believed to be a sporozoan, but later considered to be a fungus and has been provisionally placed under the Family -Olipidiaceae, Order -chytridiales of phycomyetes by ASHWORTH. Recently, Some consider it to be a protozoa or a fish parasite belonging to DRIP clade (Dermocystidium, Rosette agent,Ichthyophonus and Psorospermum).

4. MODE OF TRANSMISSION & SPREAD Transmitted while bathing in ponds with contaminated water. Theories of spread Demellow's theory of direct transmission- By direct contact of nasal mucosa Autoinoculation theory of Karunarathnae (responsible for satellite lesions). Haematogenous spread - to distant sites Lymphatic spread - causing lymphadenitis (rare).

5. LIFE CYCLE Three stages have been recognized in the life cycle of the organism: trophic stage, development of sporangia and production of endospores

6. LIFE CYCLE A - Trophozoite (juvenile sporangium) B & C - Immature bilamellar sporangia D & E - intermediate sporangia with centrifugal and centripetal maturation of endospores F - Mature sporangium with spores exiting through the operculum G - Free endospore with residual mucoid material giving it a comet like appearance (comet of Beattie) H - Free electorn body (ultimate infective unit) J - Free electron dense body surrounded by other electron dense bodies which are nutritive granules.

7. The cardinal features of rhinosporidiosis are 1. chronicity 2. recurrence 3. dissemination The reasons for chronicity are 1.Antigen sequestration - The chitinous wall and thick cellulose inner wall surrounding the endospores is impervious to the exit of endosporal antigens from inside, and is also impermeable to immune destruction. 2. Antigenic variation 3. Immunosuppression - possible release of immunosuppressive agents 4 Immune distraction 5. Immune deviation 6. Binding of host immunoglobulins .

8. CLINICAL CLASSIFICATION Nasal Nasopharyngeal Mixed Bizarre (ocular and genital) Malignant rhinosporidiosis (cutaneous rhinosporidiosis)

9. CLINICAL FEATURES The disease mostly affects nose and nasopharynx; other sites such as lip, palate, conjunctiva, epiglottis, larynx, trachea,bronchi, skin, vulva and vagina may also be affected. In the nose, the disease presents as a leafy, polypoidal mass - pink to purple in colour attached to nasal septum or lateral wall Sometimes it extends into the nasopharynx and may hang behind the soft palate. The mass is very vascular and bleeds easily on touch. Its surface is studded with white dots representing the sporangia of fungus. In early stages, the patient may complain of nasal discharge which is often blood tinged and nasal stuffiness. Sometimes, frank epistaxis is the only presenting complaint

10. Cutaneous Manifestations 3 types of skin lesions are seen a)satellite lesions- in which skin adjacent to the nasal rhinosporidiosis is involved secondarily. b)generalised cutaneous lesions-occurring through hematogenous dissemination of the organism. c)primary cutaneous lesions-associated with direct inoculation of organisms on to the skin. Cutaneous rhinosporidiosis may also present as warty papules and nodules with whitish spots, crusting, and bleeding on the surface.

11. DIAGNOSIS This is made on biopsy. It shows several sporangia, oval or round in shape and filled with spores which may be seen bursting through its chitinous wall. It has to be differentiated from coccidiomycosis- sporangia are smaller in size

12. DIAGNOSIS The role of imaging in rhinosporidiosis is to evaluate the number of lesions, the location and extent of disease, surrounding bone involvement, nasolacrimal duct involvement, and any associated complications .

13. TREATMENT Not many drugs are effective against the disease. Dapsone has been tried with some success. While several antibacterial and antifungal drugs have been tested clinically, the only drug which was found to have some anti-rhinosporidial effect is dapsone (4,4- diaminodiphenyl sulphone) which appears to arrest the maturation of the sporangia and to promote fibrosis in the stroma, when used as an adjunct to surgery. Dose of Dapsone- 100 mg once daily for 6 months to several years.Check LFT and blood counts every 2 weeks.

14. TREATMENT Complete excision of the mass with diathermy knife and cauterization of its base. Recurrence may occur after surgical excision. Pedunculated polyps radical removal Excision of sessile polyps with broad bases of attachment to the underlying tissues are sometimes followed by recurrence due to spillage of endospores on the adjacent mucosa. Smaller lesions may be removed by CO2 Laser

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