Rhinosporidiosis is a chronic infection caused by Rhinosporidium seeberi, affecting mainly India and Sri Lanka. It most commonly presents as polypoidal lesions in the nose and nasopharynx. Microscopically, sporangia containing endospores are seen. Treatment involves surgical excision and dapsone medication to prevent recurrence due to the organism's ability to disseminate via blood and lymphatics. Recurrence is common if all infected tissue is not removed.
2. • Introduction
• History
• Incidence
• Mode of spread
• Life cycle
• Cardinal features
• Clinical manifestations
• Investigations
• Treatment.
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3. Introduction
• Rhinosporidiosis is a chronic granulomatous infective disorder caused by
Rhinosporidium seeberi, whose taxonomy is still debated
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Sinha A, Phukan JP, Bandyopadhyay G, et al. Clinicopathological study of rhinosporidiosis with special reference to
cytodiagnosis. J Cytol. 2012;29(4):246–249. doi:10.4103/0970-9371.103943
4. History &Taxonomy
• 1892- regarded as a sporozoan by Malbran, its discoverer, in nasal polyp
• 1900- Protozoan by Guillermo Seeber who first published a description of the
pathogen
• 1923- Phycomycete by Ashworth
• Herr et al classified the organism in a new clade -Mesomycetozoa, which includes
fish and amphibian pathogens in the former DRIP clade (Dermocystidium, the
rossette agent, Ichthyophonus and Psorospermium).
• 1953 - Demellow described the mode of its transmission
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Indian Journal of Medical Microbiology, (2002) 20 (3):119-131
5. INCIDENCE AND GEOGRAPHICAL DISTRIBUTION
India and Sri Lanka.
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Sinha A, Phukan JP, Bandyopadhyay G, et al. Clinicopathological study of rhinosporidiosis with special reference to
cytodiagnosis. J Cytol. 2012;29(4):246–249. doi:10.4103/0970-9371.103943
6. Hypothesized Mode of Spread
Theories
• Demellow's theory of direct transmission.
• Autoinoculation theory of Karunarathnae (responsible for satellite lesions).
• Haematogenous spread - to distant sites
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Prakash M, Johnny JC. Rhinosporidiosis and the pond. J Pharm Bioallied Sci. 2015;7(Suppl 1):S59–S62.
doi:10.4103/0975-7406.155804
7. Classifications
• Nose and nasopharynx were the most commonly affected sites (74.6%),
• followed by eye (19%).
• Other rare sites accounted for (6.3%)
Lips, Palate, Uvula, Maxillary Antrum, Epiglottis, Larynx, Trachea, Bronchus,
Ear, Scalp, Vulva, Penis, Rectum and Skin
DEPARTMENT OF OTORHINOLARYNGOLOGY,
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Sinha A, Phukan JP, Bandyopadhyay G, et al. Clinicopathological study of rhinosporidiosis with special reference to
cytodiagnosis. J Cytol. 2012;29(4):246–249. doi:10.4103/0970-9371.103943
8. Reasons for endemicity:
• Aquatic micro-organisms might also be relevant to a possible synergistic action in
the establishment of natural rhinosporidiosis. *
• Blood group studies indicate that rhinosporidiosis is common in patient's with
group O (70%), the next high incidence was in group AB.**
• Cultureal practice**
• Climatic conditions**
• Physiochemical properties of water**
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*Indian Journal of Medical Microbiology, (2002) 20 (3):119-131
**Prakash M, Johnny JC. Rhinosporidiosis and the pond. J Pharm Bioallied Sci.
2015;7(Suppl 1):S59–S62. doi:10.4103/0975-7406.155804
10. Cardinal features
The cardinal features of rhinosporidiosis are
1. Chronicity
2. Recurrence
3. Dissemination
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11. REASONS FOR CHRONICITY
• Antigen sequestration
• Antigenic variation
• Immune suppression
• Immune distraction
• Binding of host immunoglobulins
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12. Clinical manifestations
DEPARTMENT OF OTORHINOLARYNGOLOGY,
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Sinha A, Phukan JP, Bandyopadhyay G, et al. Clinicopathological study of rhinosporidiosis with special reference to
cytodiagnosis. J Cytol. 2012;29(4):246–249. doi:10.4103/0970-9371.103943
13. Karthikeyan P, Vijayasundaram S, Pulimoottil
DT. A Retrospective Epidemiological Study
of Rhinosporidiosis in a Rural Tertiary Care
Centre in Pondicherry. J Clin Diagn Res.
2016;10(5):MC04–MC8.
doi:10.7860/JCDR/2016/17465.7788
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14. Gross features
DEPARTMENT OF OTORHINOLARYNGOLOGY,
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Sinha A, Phukan JP, Bandyopadhyay G, et al. Clinicopathological study of rhinosporidiosis with special reference to
cytodiagnosis. J Cytol. 2012;29(4):246–249. doi:10.4103/0970-9371.103943
15. • HISTOLOGY
DEPARTMENT OF OTORHINOLARYNGOLOGY,
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Sinha A, Phukan JP, Bandyopadhyay G, et al. Clinicopathological study of rhinosporidiosis with special reference to
cytodiagnosis. J Cytol. 2012;29(4):246–249. doi:10.4103/0970-9371.103943
16. Investigations
• Histology is the mainstay of diagnosis.
• A diagnosis of the disease can be made by simple aspiration cytology, the
examination of aspirated material with Gomori methenamine silver and periodic
acid–Schiff reaction, and the presence of the organism indifferent stages of
maturation even in the absence of a histopathological study.
• It has to be differentiated from coccidiomycosis.
• Endospores of coccidiomycosis have sporangia of smaller size.
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17. TREATMENT
• SURGICAL – endoscopic excision and cauterization of the base
-laser excision
• MEDICAL
Dose of Dapsone- 100 mg once daily for 6 months to several
years.Check LFT and blood counts every 2 weeks.
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18. Conclusion
• Rhinosporidiosis shows both long duration & tendency for recurrence.
• Recurrent seeding of circulation with spores from nose & nasopharynx may lead
to involvement of non mucosal sites.
• Trans epithelial infection is also important for recurrence in sites & extension to
nearby sites.
• Failure to remove all infected tissues at the time of surgery & implantation of
spores in fresh areas of abrasions may cause recurrence.
• Removal of growth by snare without cauterisation was considered to result in
dissemination & recurrence.
• Good result obtained with diathermy was explained on the basis that it avoids
implantation of spores & destruction is deep.
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R seeberi, aquatic protozoan previously considered to be a fungus. Infection affects nasal mucous membranes and ocular conjunctivae of humans and animals, producing slowly growing masses that degenerate into polyps.
Through molecular biological analysis of the organism’s ribosomal DNA
known to medicine since 1900 following its first description by Guillermo Seeber in Buenos Aires, Argentina, who proposed the infective aetiology for this disease to be a fungus, which was later isolated by Ashworth in 1923, who in turn described the life cycle of the organism and established the nomenclature Rhinosporidium seeber
Male have more outdoor activities
Demellow.s- He postulated that infection always occured as a result of direct transmission of the organsim.
Karunarathnae accounted for satellite lesions in skin and conjunctival mucosa as a result of auto inoculation.
Karunarathnae also postulated that Rhinosporidium existed in a dimorphic state.
There are examples of such synergism of bacteria, with parasites - lactobacilli with Trichomonas, and Wolbachia with filarial nematode
Spore or spherule-
comet of Beattee. 7a- electron dense bodies 7b-electron dense bodies surrounded by nutritive granule.
4a,b- centrifugal and centripetal maturation of endospores
Though anti-rhinosporidial humoral and cell mediated immune responses do occur in human rhinosporidiosis, there are indications that R.seeberi evades specific adaptive immunity through several mechanisms which might explain some hitherto(until now) enigmatic(mysterious) aspects of rhinosporidiosis viz., chronicity, recurrence and dissemination:
Antigenic sequestration- impervious to exit of endosporal antigen and also immune destruction
Immune supprestion – possible release of immune suppressor agents
Lesions in the nose can be polypoidal, reddish and granular masses. They could be multiple pedunculated and friable. They are highly vascular and bleed easily. Their surface is studded with whitish dots (sporangia)
Histopathological sections show multiple sporangia in various stages of maturity, enclosed in a thin chitinous wall. The sporangia are 50-1000 µm in diameter, containing numerous endospores of diameter 5-10 µm. Overlying epithelium is usually hyperplastic and loose fibrovascular stroma infiltrated with lymphocytes, macrophages, plasma cells and even polymorphonuclear leucocytes