Indian Journal of Dermatology
E-IJD CORRESPONDENCE
Year
: 2015  |  Volume : 60  |  Issue : 2  |  Page : 218-

Disseminated cutaneous rhinosporidiosis: a polymorphic presentation in an immunocompetent patient


Bharati Sahu, Puspanjali Sahu, Manas R Puhan 
 From the Department of Skin and Venereal Diseases, Shrirama Chandra Bhanj Medical College, Cuttack, Odisha, India

Correspondence Address:
Bharati Sahu
From the Department of Skin and Venereal Diseases, Shrirama Chandra Bhanj Medical College, Cuttack, Odisha
India




How to cite this article:
Sahu B, Sahu P, Puhan MR. Disseminated cutaneous rhinosporidiosis: a polymorphic presentation in an immunocompetent patient.Indian J Dermatol 2015;60:218-218


How to cite this URL:
Sahu B, Sahu P, Puhan MR. Disseminated cutaneous rhinosporidiosis: a polymorphic presentation in an immunocompetent patient. Indian J Dermatol [serial online] 2015 [cited 2021 Sep 21 ];60:218-218
Available from: https://www.e-ijd.org/text.asp?2015/60/2/218/152596


Full Text

Sir,

A 65-year-old female presented with asymptomatic lumps, two in number on her left antero-lateral thigh of 10 months duration. On examination the larger nodule was of size 16 × 12 cm with a smooth surface, firm to soft in consistency and with dilated veins over it. It was not attached to underlying structures, with minimal signs of inflammation. The smaller nodule (5 × 5 cm) was highly tender, soft in consistency giving a pyogenic granuloma-like appearance at the site of rupture [Figure 1]. There was a history of nasal mass with recurrent epistaxis 6 months back, excised but without any record. The patient used to take bath in pond daily. General physical and systemic examinations were within normal limits. Routine hemogram was within normal limits. Chest X-ray and abdominal ultrasonography were within normal limits. ELISA for HIV was non-reactive. Radiological evaluation revealed a clearly delineated dense radiopaque subcutaneous mass not attached to underlying structures. A biopsy from the lesion showed immature and mature thick-walled sporangia with endospores in highly vascular sub-epithelial stroma and dermis, respectively [Figure 2]. Few sporangia rupturing to release the endospores were also seen [Figure 3].{Figure 1}{Figure 2}{Figure 3}

Diagnosis of disseminated cutaneous rhinosporidiosis along with nasal rhinosporidiosis was made. Lesions were excised with electrocoagulation of the base and dapsone was given to prevent recurrence.

Rhinosporidiosis is a rare chronic granulomatous condition, acquired by contact with stagnant water like ponds and swimming pools. Rhinosporidium seeberi, etiological agent for rhinosporidiosis, was initially classified as a fungus. A portion of the R. seeberi 18S rRNA gene was amplified using PCR which supports its phylogentic relationship with protozoa, now classified as an aquatic protistan of Mesomycetozoea class (Ichthyosporea). [1] It is endemic in Sri Lanka and parts of India. In India Orissa, Chhattisgarh, Tamil Nadu, Kerala, Karnataka, and Pondicherry are endemic states for this disease. Sporadic cases among migrant population are seen. [2],[3] Four common varieties have been described nasal, ocular, cutaneous, and disseminated forms. [4],[5],[6],[7],[8],[9] Cutaneous lesions are very rare, and generally associated with simultaneous or with past history of mucosal lesions.

Three main types of cutaneous rhinosporidiosis and their mode of spread had been reported:

1. Satellite skin lesions surrounding mucosal lesions through autoinoculation.

2. Disseminated skin lesions with or without the nasal involvement through a hematogenous route.

3. Primary cutaneous type through direct inoculation.

Mucosal lesions develop through transepithelial spread. [10],[11] Skin lesions resembling lipomas, verrucous tuberculosis, pyogenic granulomas, viral wart, donovanosis and also subcutaneous nodules have been described. Other rarer forms include those resembling soft tissue tumors, furuncles, ecthyma, and giant cutaneous lesions. Treatment is by excision with electrocoagulation, but recurrences may occur. Oral dapsone might arrest the maturation of the sporangia and cause stromal fibrosis. [12]

Our patient had disseminated cutaneous rhinosporidiosis without any evidence of immunosuppression. She had polymorphic lesions, an asymptomatic subcutaneous giant mass, and a smaller painful pyogenic granuloma like lesion. Only two cases of polymorphic lesions in a single patient had been described earlier. [13] This case is being reported due to rare polymorphic lesions of rhinosporidiosis in an immunocompetent patient.

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