Rhinosporidiosis: A case report with review of literature


Rhinosporidiosis is a chronic infestation by the fungus Rhinosporidium seeberi, which predominantly affects the mucus membranes of the nose and nasopharynx. We report a case of rhinosporidiosis with presentation as a mass extending up to the oropharynx. Functional endoscopic sinus surgery was performed.

Keywords: Endospores, mass, oropharynx, rhinosporidiosis

How to cite this article:
Babu S, Anuradha A, Chandra S, Kashyap B. Rhinosporidiosis: A case report with review of literature. Ann Trop Med Public Health 2012;5:127-9
How to cite this URL:
Babu S, Anuradha A, Chandra S, Kashyap B. Rhinosporidiosis: A case report with review of literature. Ann Trop Med Public Health [serial online] 2012 [cited 2021 Mar 6];5:127-9. Available from: https://www.atmph.org/text.asp?2012/5/2/127/95969

Rhinosporidium is a cosmopolitan disease of man and domestic animals endemic in India and Sri Lanka and is hyperendemic in southern districts of Tamil Nadu. It usually presents as a polypoidal growth in nasal cavity that involves anterior part of nasal septum and nasal vestibule.

Case Report

A 42-year-old male from Orissa, professionally a farmer, came to the outpatient department with a complaint of foreign body sensation in the throat present since 4 years and nasal obstruction for the past 6 years. He was also suffering from recurrent episodes of headache and dysphasia for past 6 months. There was occasional history of otalgia and epistaxis. His medical history was noncontributary. Anterior rhinoscopy showed bilateral pinkish polypoidal mass filling both the nasal cavities [Figure 1]. The nasal mucosa was swollen, hyperemic, and covered with copious viscid secretion. The erythematous polypoidal mass was 5 x 4 cm and was extending through the nasopharynx and hanging into the oropharynx up to the level of the posterior one-third of the tongue along the posterior pharyngeal wall [Figure 2]. It was non-pulsating or expansile, did not bleed on touch. Lymph nodal involvement was absent. CT scanning revealed haziness of the maxillary sinus with bilateral hyperdense mass filling the nasal cavities with oropharyngeal extension [Figure 3] and [Figure 4]. A differential diagnosis of infected polyp, inverted ductal papilloma, and fungal proliferation was given. Functional endoscopic sinus surgery was performed and the nasopharyngeal mass was excised and the tissue was sent for histopathological examination [Figure 5].

Figure 1: Bilateral pinkish mass filling the nasal cavities prominent on the left

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Figure 2: Reddish-pink irregular mass in the oropharynx

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Figure 3: CT picture shows bilateral nasal mass with bilateral maxillary sinus haziness

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Figure 4: CT picture shows oropharyngeal extension of the mass

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Figure 5: Excised mass

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The specimen on gross examination was polypoidal, soft, friable, and pink in color with white spots on the surface. Histopathological examination of tissue sections stained with hematoxylin and eosin (HandE) and periodic acid-Schiff (PAS) stain showed a surface stratified squamous epithelium. The subepithelium showed many globular cysts. Each of these cysts represented a thick-walled sporangium containing numerous “daughter spores” in different stages of development. The fibrous connective stroma showed fibroblasts and an inflammatory infiltrate consisting of polymorphs and eosinophils [Figure 6] and [Figure 7]. These changes were characteristic of rhinosporidiosis.

Figure 6: Hematoxylin and eosin tissue sections lined by stratified squamous epithelium and subepithelial thick-walled globular cysts containing numerous daughter spores in different stages of development

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Figure 7: Periodic acid Schiff-stained sections demonstrating the sporangia in a fibromyxoid stroma containing polymorphs and eosinophils

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The first known case of rhinosporidiosis was identified in 1892 by Malbran of Buenos Aires. Seeber published the first detailed account of rhinosporidiosis in 1900. In 1923, Ashworth described the fungus’ life cycle, and in 1964, Karunaratne published a complete review of rhinosporidiosis in man. Other than India and Sri Lanka where this disease is endemic, it has been recognized in many other parts of the world, like South America, United states, England, Egypt, and South Africa.

Rhinosporidiosis predominantly affects the mucous membranes of the nose and nasopharynx; it also occasionally involves the lips, palate, uvula, maxillary antrum, conjunctiva, lacrimal sac, epiglottis, larynx, trachea, bronchus, ear, scalp, skin, penis, vulva, and vagina. Water and soil are believed to be the reservoir of infection, given the increased incidence of disease found in sand workers, paddy cultivators, and people bathing in stagnant muddy waters. Mode of transmission is through water or dust, from which the endospores penetrate the nasal mucosa, mature into sporangium within the submucosal compartment, and after maturation burst with release of sporangia into surrounding tissue. Clinically, the lesion presents as a soft, polypoid, mass sometimes pedunculated in the nose, the eye and its adnexa, conjunctiva, or the urethra. Larynx, trachea, skin, and lung are less frequently involved. Osteolytic bone infiltration is another clinical presentation. Histologically, the infected tissue reveals granulomatous reaction, pseudocystic abscesses, and fibrosis around the causative organism. [1],[2],[3]

The taxonomy of the causative organism is unclear. It shows morphological features resembling those of fungi and protozoa. Though most microbiologists had initially considered it a fungus as fungal stains such as methanamine silver and PAS could stain the wall of the organism, but culture of Rhinosporidium seeberi had been unsuccessful in all artificial media; however, it could be maintained through its life cycle in tissue cultures. Recently, Ahluwalia hypothesized that the causative organism was not a fungus, but a prokaryotic cyanobacterium Microcystis aeruginosa, based on the findings that this organism was isolated from both the clinical specimens of patients and the pond water samples where they bathed. [4],[5],[6] Herr et al., however, through analysis of the 18S small subunit ribosomal DNA groups, concluded that R. seeberi was related to a group of fish parasites referred to as the DRIP clade. [7] The biological agent has a mature stage that consists of large, thick-walled spherical structures (called sporangia) containing smaller “daughter cells” (called “sporangiospores”), and it can be visualized with fungal stains such as Gomori methenamine silver and PAS, as well as with standard HandE staining.

Surgical excision is the mainstay of treatment. It has been advocated that a wide surgical margin is necessary to reduce the risk of recurrence, though this may be associated with significant morbidity like hemorrhage and nasal septal perforation. Because of this, limited surgical excision with cautery of the base of the lesion has been attempted, and to further reduce the risk of recurrence, various adjuvant medical therapies, including antifungals such as griseofulvin and amphotericin B, have been tried without much success. The only drug appearing to have clinical promise is dapsone. [8],[9],[10]


Rhinosporidiosis is a condition which both clinicians and laboratory personnel should keep in mind, particularly when managing masses in the nasal cavity in patients from endemic places.

1. Loh KS, Chong SM, Pang YT, Soh K. Rhinosporidiosis: Differential diagnosis of a large nasal mass. Otolaryngol Head Neck Surg 2001;124:121-2.
2. Arseculeratne SN. Microcystis aeruginosa as the causative organism of rhinosporidiosis. Mycopathologia 2000;151:3-4.
3. Fredricks DN, Jolley JA, Lepp PW, Kosek JC, Relman DA. Rhinosporidium seeberi: A human pathogen from a novel group of aquatic protistan parasites. Emerg Infect Dis 2000;6:273-82.
4. Ahluwalia KB. Culture of the organism that causes rhinosporidiosis. J Laryngol Otol 1999;113:523-8.
5. Ahluwalia KB, Maheshwari N, Deka RC. Rhinosporidiosis: A study that resolves etiologic controversies. Am J Rhinol 1997;11:479-83.
6. Ahluwalia KB. New interpretations in rhinosporidiosis, enigmatic disease of the last nine decades. J Submicrosc Cytol Pathol 1992;24:109-14.
7. Herr RA, Ajello L, Taylor JW, Arseculeratne SN, Mendoza L. Phylogenetic analysis of Rhinosporidium seeberi’s 18S small subunit ribosomal DNA groups this pathogen among members of the protoctistan Mesomycetozoa clade. J Clin Microbiol 1999;37:2750-4.
8. Nair KK. Clinical trial of diaminodiphenylsulfone (DDS) in nasal and nasopharyngeal rhinsporidiosis. Laryngoscope 1979;89:291-5.
9. Job A, Venkateswaran S, Mathan M, Krishnaswami H, Raman R. Medical therapy of rhinosporidiosis with dapsone. J Laryngol Otol 1993;107:809-12.
10. Venkateswaran S, Date A, Job A, Mathan M. Light and electron microscopic findings in rhinosporidiosis after dapsone therapy. Trop Med Int Health 1997;2:1128-32.

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.95969


[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]

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