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Q1: WHAT IS YOUR DIAGNOSIS?
The diagnosis is cutaneous rhinosporidiosis. The patient gave past history of reddish polyps in the nostrils. He had a reddish friable mass in the nasopharynx and verrucous cutaneous lesions with haemorrhagic spots on top. The possible differential diagnosis1 is listed in box 1.
Box 1: Differential diagnosis
Donovanosis (genital lesions).
Condyloma acuminata (genital lesions).
Cutaneous rhinosporidiosis may present as warty papules and nodules with whitish spots, crusting and bleeding on the surface.
Careful inspection of the surface of the warty lesions and the presence of typical nasopharyngeal lesions helps in suspecting cutaneous rhinosporidiosis.
The diagnosis can be confirmed by demonstrating typical sporangia and spores in histopathology and imprint smears.
Surgical removal and electrodesiccation are the treatments of choice.
Dapsone supplementation may arrest the maturation of sporangia and accelerate degenerative changes in them.
Q2: HOW CAN YOU CONFIRM YOUR DIAGNOSIS?
Giemsa stained imprint smears taken from the surface of the lesion showing typical sporangia can easily clinch the diagnosis.1 Scrape cytology of the lesion demonstrates typical spherical spores of variable sizes with transparent capsules, and eosinophilic globular bodies (8–10) within the spores in haematoxylin and eosin or Papanicolaou stained smears.2 Fine needle aspiration cytology from the lesion could be an additional diagnostic tool.1
Histopathology reveals enormous numbers of mycotic elements in the subepithelial connective tissue. These consist of sharply defined globular thick walled cysts (sporangia) up to 0.5 mm in diameter, which contain numerous rounded endospores, 6–7 μm in diameter. Immature and collapsed sporangia are also present. Occasionally, microabscesses may be formed.3, 4
Q3: WHAT IS THE TREATMENT OF THIS DISEASE?
Rhinosporidiosis is a chronic granulomatous mycosis caused by Rhinosporidium seeberi. The organism has never been isolated in vitro and its taxonomic position is not clear.4 Cultivation in an epithelial cell line and in standard media at a pH of 5.8 to 6.5 under an optimum temperature of 23°C has been reported.3 The disease is endemic in India and Sri Lanka, but has also been reported from the United States of America, South America, and Iran.1, 3 It is more common in adult males and is possibly transmitted to man by direct contact with spores through dust, infected clothing or fingers, and swimming in stagnant waters.2, 3
Rhinosporidiosis frequently involves the nasopharynx (70%) presenting as a painless, friable, polypoidal growth, which may hang, anteriorly from the nares or posteriorly into the pharynx.1, 5 The lesions are pink or purple red and studded with minute white spots, which are the sporangia containing spores.1, 3 Nasal obstruction and bleeding are the most common symptoms.5 The conjunctiva and lacrimal sac are involved in 15% of cases. Occasionally, it affects the lips, palate, uvula, maxillary antrum, epiglottis, larynx, trachea, bronchus, ear, scalp, vulva, vagina, penis, rectum, or the skin.3 The infection is usually limited to the surface epithelium, but rarely wide dissemination with visceral involvement can occur.3
Cutaneous lesions are not very common and usually start as friable papillomas that become pedunculated.1, 3 Cutaneous rhinosporidiosis may also present as warty papules and nodules with whitish spots, crusting and bleeding on the surface.3 Three types of skin involvement can occur1, 3: (1) satellite lesions, in which skin adjacent to the nasal rhinosporidiosis is involved secondarily; (2) generalised cutaneous type with or without nasal involvement, occurring through haematogenous dissemination of the organism; and (3) primary cutaneous type, due to direct inoculation of organisms on to the skin.
Careful inspection of the surface of the warty lesions and the presence of typical nasopharyngeal lesions helped in suspecting cutaneous rhinosporidiosis in our case. Since the causative agent cannot be cultured, the diagnosis can be confirmed by demonstrating typical sporangia and spores in histopathology and imprint smears.1, 4 Surgical removal and electrodesiccation are the treatments of choice.3, 5 Dapsone may arrest the maturation of sporangia and accelerate degenerative changes in them. The effete organisms are then removed by an accelerated granulomatous response. For the same reasons, dapsone has been used to reduce postoperative recurrences as well.3
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