Rhinosporidiosis is a chronic granulomatous infection of the mucous membranes that usually manifests as vascular friable polyps that arise from the nasal mucosa or external structures of the eye.
History:
1892 – Malbran observed the organism in nasal polyp
1900 – Seeber described the organism
1903 – O’Kineley described its histology
1905 – Minchin & Fantham studied O’Kineley’s tissue and named the organism as Rhinosporidium Kinealyi
1913 – ZSchokke reported similar organism in horses and named it Rhinosporidium equi
1923 – Ashworth described its life cycle
1924 – Forsyth described skin lesion
1924 – Thirumoorthy reported the first female patient
1936 – Cefferi establised the identity of R. Seeberi and R. Equi
1953 – Demellow described the mode of its transmission
Initially described by Seeber in 1900 in an individual from Argentina, rhinosporidiosis is endemic in India, Sri Lanka, South America, and Africa. Cases from the United States and Southeast Asia, as well as scattered occurrences throughout the world, have also been reported. Most cases of rhinosporidiosis occur in persons from or residing in the Indian subcontinent or SriLanka. In addition to humans, disease has been noted in cats, cattle, dogs, ducks, goats, horses, mules, parrots, and swan.
The etiologic agent, Rhinosporidium seeberi, has never been successfully propagated in vitro. Initially thought to be a parasite, for more than 50 years R seeberi had been considered a water mold.
Molecular biological techniques have more recently demonstrated this organism to be an aquatic protistan parasite, and it has been placed into a new class, the Mesomycetozoea, along with organisms that cause similar infections in amphibians and fish. This reclassification is not without controversy, as other researchers have presented data that R seeberi is a cyanobacterium, further demonstrating the difficulties that arise when working with pathogens that cannot be maintained in the laboratory setting. Other molecular work has demonstrated evidence that R seeberi may have host-specific strains (eg, human vs dog versus swan).
Pathophysiology
Rhinosporidiosis is an infection that is typically limited to the mucosal epithelium. Infection usually results from a local traumatic inoculation with the organism. 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 observed in 70% of persons with rhinosporidiosis; infection of the palpebral conjunctivae or associated structures (including the lacrimal apparatus) is observed in 15%.
Common sites affected:
Nose – 78%
Nasopharynx – 68%
Tonsil – 3%
Eye – 1%
Skin – very rare
Other structures of the mouth, upper airway, and eye may be sites of disease. Disease of the skin, ear, larynx, trachea, bronchi, genitals, and rectum has also been described. disease has been described in the vagina, penile urethra or meatus, and scrotum. Dissemination with cutaneous and multisite disease is also reported, but this is much less common. Isolated cases of dissemination involving deep organs have been rarely reported
Theories of mode of spread:
Autoinoculation theory of Karunarathnae (responsible for satellite lesions)
Haematogenous spread – to distant sites
Lymphatic spread – causing lymphadenitis (rarity)
Demellow’s theory of direct transmission – This theory propounded by Demellow had its acceptance for quite sometime. He postulated that infection always occured as a result of direct transmission of the organsim. When nasal mucosa comes into contact with infected material while bathing in common ponds, infection found its way into the nasal mucosa.Karunarathnae accounted for satellite lesions in skin and conjunctival mucosa as a result of auto inoculation.Rhinosporidiosis affecting distant sites could be accounted for only through haematogenous spread.Karunarathnae also postulated that Rhinosporidium existed in a dimorphic state. It existed as a saprophyte in soil and water and it took a yeast form when it reached inside the tissues. This dimorphic capability helped it to survive hostile environments for a long period of time.
Reasons for endemicity of Rhinosporidiosis:
It has to be explained why this disease is endemic in certain parts of South India and in the dry zone of Srilanka. If stagnant water could be the reason then the chemical and physical characteristics of the water needs to be defined. In addition other aquatic organisms may also be playing an important synergistic reaction. This aspect need to be elucidated. Text book of microbilogy is repleate with examples of such synergism i.e. lactobacillus with trichomonas, and Wolbachia with filarial nematodes.
Host factors responsible for endemicity: Eventhough quite a large number of people living in the endemic areas take bath in common ponds only a few develop the disease. This indicates a predisposing, though obscure factors in the host. Blood group studies indicate that rhinosporidiosis is common in patient’s with group O (70%), the next high incidence was in group AB. Jain reported that blood group distribution is too variable to draw any conclusion. Larger series must be studied for any meaningful analysis. HLA typing also must be studied. The possibility of non-specific immune reactivity especially macrophages in protecting the individual from Rhinosporidium seeberi must be considered.
History
Unilateral nasal obstruction
Epistaxis
Local pruritus
Rhinorrhea
Coryza with sneezing
Post nasal discharge with cough
Foreign body sensation
History of exposure to contaminant water
Increased tearing and photo phobia in cases of infection of palpebral conjunctiva
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). They can be clearly seen with a hand lens. The whole mass is covered by mucoid secretion. The rhinosporidium in the nose is restricted to the nasal mucous membrane and doesnot cross the muco cutaneous barrier.
On examination
Strawberry like appearance
Bleeds easily upon manipulation
confirmed by biopsy and histopathology – several round or oval sporangia and spores which may be seen bursting through its chitinous wall
There is papillomatous hyperplasia of nasal mucous membrane with rugae formation. The epithelium over the sporangia is thinned out, foreign body giant cells can be seen. Accumulation of mucous in the crypts seen with increased vascularity. The increased vascularity is responsible for excessive bleeding during surgery. Increased vascularity is due to the release of angiognenesis factor from the rhinosporidial mass. Rhinosporidial spores stain with sudan black, Bromphenol blue etc.
Dr. Sriharsha Tikka 