RHINOSPORIDIOSIS

Etiology & habitat: The etiological agent is Rhinosporidium seeberi. It commonly causes human infections in India, Sri Lanka, South America, and Africa. Its classification has undergone many changes; it was initially thought to be a parasite, then it was considered to be a fungus but now molecular biological techniques have demonstrated that this organism is an aquatic protistan parasite. It is currently included in a new class, the Mesomycetozoea. The disease has been sporadically reported in many countries in several animal species, including dogs, horses, donkeys, cattle, cats, geese, and ducks. The source of infection of rhinosporidiosis is not clearly determined, but it seems associated with stagnant water.

Pathogenesis: Rhinosporidium lives in soil and it is believed that water is a necessary medium of transmission. Infection usually results from a local traumatic inoculation and is associated with water activities e.g. swimming in stagnant water. The infection is typically limited to the mucosal epithelium. Its life cycle begins with a round endospore(6-10 μm in diameter), which grows to become a thick-walled sporangium (100-450 μm in diameter) that contains up to several thousand endospores. Mature sporangiospores are approximately 7-9 um in size and escape through a pore that develops in the sporangial wall. The disease progresses with the local replication of R. seeberi and associated hyperplastic growth of host tissue and a localized immune response. Infection of the nose and nasopharynx is common; other parts include palpebral conjunctivae, skin, ear, genitals, and rectum. These polyps are pink to deep red, are sessile or pedunculated, and are often described as strawberry-like in appearance. Because the polyps of rhinosporidiosis are vascular and friable, they bleed easily upon manipulation. The polyps are chronic but are not painful. They can cause obstruction of the respiratory tract resulting in asphyxia.

Laboratory diagnosis: Nasal secretion (if any) should be collected. The entire polyp must be surgically excised; some tissue may be macerated or biopsies are taken. The secretions or macerated tissue is observed under microscope with a KOH mount or after staining with H&E. Tissue sections can also be stained with GMS or PAS. The inner wall of sporangia and the outer surface of sporangiospores can be stained using Meyer's mucicarmine stain. Microscopy observations revealed presence of several spherical sporangia of various sizes containing numerous sporangiospores. H&E stained sections also reveal diffuse infiltration of lymphocytes, monocytes, and plasma cells besides sporangia. Culture is not possible since this organism has not been successfully cultivated in-vitro.

Treatment: Local surgical excision is the treatment of choice. Recurrence has been reported with simple excision.