Dr. T. Balasubramanian M.S. D.L.O.
Rhinosporidiosis has been defined as a chronic
granulomatous disease characterised by production of polyps and other
manifestations of hyperplasia of nasal mucosa. The etiological agent is
Rhinosporidium seeberi: was initially believed
to be a sporozoan, but it is now considered to be a fungus and has been
provisionally placed under the family Olipidiaceae, order chritridiales
of phycomyetes by Ashworth. More recent classification puts it under
DRIP'S clade. Even after extensive studies there is no consensus on
where Rhinosporidium must be placed in the Taxonomic classification. It
has not been possible to demonstrate fungal proteins in Rhinosporidium
even after performing sensitive tests like Polymerase chain reactions.
- 1892 - Malbran observed the organism in nasal
- 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
- 1936 - Cefferi establised the identity of R.
Seeberi and R. Equi
- 1953 - Demellow described the mode of its
Incidence and Geographical distribution:
Of all the reported cases 95 % were from India
and Srilanka. An all India survey conducted in 1957 revealed that this
disease is unknown in states of Jummu & Kashmir, Himachal pradesh,
Punjab, Haryana, and North Eastern states of India. In the state of
TamilNadu 4 endemic areas have been identified in the survey, (Madurai,
Ramnad, Rajapalayam, and Sivaganga). The common denominator in these
areas is the habit of people taking bath in common ponds.
Right nasal rhinosporidial mass (strawberry like mulberry mass)
Theories of mode of spread:
- Demellow's theory of direct transmission
- Autoinoculation theory of Karunarathnae
(responsible for satellite lesions)
- Haematogenous spread - to distant sites
- Lymphatic spread - causing lymphadenitis
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.
Life cycle: (Ashworth) Spore is the ultimate
infecting unit. It measures about 7 microns, about the size of a red
cell. It is also known as a spherule. It has a clear cytoplasm with 15
- 20 vacuoles filled with food matter. It is enclosed in a chitinous
membrane. This membrane protects the spore from hostile environment. It
is found only in connective tissue spaces and is rarely intracellular.
The spore increases in size, and when it reaches
50 - 60 microns in size granules starts to appear, its nucleus prepares
for cell division. Mitosis occurs and 4, 8, 16, 32 and 64 nuclei are
formed. By the time 7th division occurs it becomes 100 microns in size.
A fully mature sporangia measures 150 - 250 microns. Mature spores are
found at the centre and immature spores are found in the periphery. The
full cycle is completed within the human body.
Diagramatic representation of Rhinosporidium seeberi as suggested by
Life cycle (recent): Since rhinosporidium
seeberi has defied all efforts to culture it, any detail regarding its
life cycle will have to be taken with a pinch of salt. This life cycle
has been postulated by studying the various forms of rhinosporidium
seen in infected tissue.
Trophozoite / Juvenile sporangium - It is 6 -
100 microns in diameter, unilamellar, stains positive with PAS, it has
a single large nucleus, (6micron stage), or multiple nuclei (100
microns stage), lipid granules are present.
Intermediate sporangium - 100 - 150 microns in
diameter. It has a bilamellar wall, outer chitinous and inner
cellulose. It contains mucin. There is no organised nucleus, lipid
globules are seen. Immature spores are seen within the cytoplasm. There
are no mature spores.
Mature sporangium - 100 - 400 microns in
diameter, with a thin bilamellar cell wall. Inside the cytoplasm
immature and mature spores are seen. They are found embedded in a
mucoid matrix. Electron dense bodies are seen in the cytoplasm. The
bilamellar cell wall has one weak spot known as the operculum.
Maturation of spores occur in both centrifugal and centripetal fashion.
This spot does not have chitinous lining, but is lined only by a
cellulose wall. The mature spores find their way out through this
operculum on rupture. The mature spores on rupture are surrounded by
mucoid matrix giving it a comet appearance. It is hence known as the
comet of Beattee
Mature spores give rise to electron dense bodies
which are the ultimate infective unit.
Diagramatic representation of life cycle of Rhinosporidiun seeberi (New)
1 - Trophozoite (juvenile sporangium)
2 & 3 - Immature bilamellar sporangia
4a & 4b - intermediate sporangia with
centrifugal and centripetal maturation of endospores
5 - Mature sporangium with spores exiting
through the operculum
6 - Free endospore with residual mucoid material
giving it a comet like apperance (comet of Beattie)
7a - Free electorn body (ultimate infective unit)
7b - Free elecctron dense body surrounded by
other electron dense bodies which are nutritive granules
Clincial classification of Rhinosporidiosis:
- Bizzarre (ocular and genital)
- Malignant rhinosporidiosis (cutaneous
Pic showing naso pharyngeal rhinosporidial mass
Pic showing rhinosporidial mass in oropharynx
Common sites affected:
- Nose - 78%
- Nasopharynx - 68%
- Tonsil - 3%
- Eye - 1%
- Skin - very rare
Gross features of rhinosporidiosis:
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.
Histopathology of nasal rhinosporidiosis:
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.
Rhinosporidial spores as seen in high power microscope
Endospores represent asexual spores of
Rhinosporidium seeberi. After nuclear division in the juvenile
sporangia, endospores are forrmed by condensation of cytoplasm around
the nuclei with the formation of cell walls. This process is known as
endosporulation. These endospores have been postulated to develop from
the inner sporangial wall. Endospores are liberated from the sporangium
by bing shot out from the sporangium after its rupture (as suggested by
Beattee), or through the operculum as suggested by Ashworth, or by
osmotic mechanism as suggested by Demello. Endospores are thick walled
measuring about 7 microns in diameter, round in shape and stains with
PAS. It has a vesicular nucleus and a granular cytoplasm. The
peripheral cytoplasm is vacuolated containing deeply staining bodies
called as spherules. These bodies give the spore a morullated
appearance and hence the term spore morullae.
Features of rhinosporidiosis:
The cardinal features of rhinosporidiosis are 1.
chronicity, 2. recurrence and 3. dissemination.
The reasons for chronicity are
1. Antigen sequestration - The chitinous wall
and thick cellulose inner wall surrounding the endospores is impervious
to the exit of endosporal antigens from inside, and is also impermeable
to immune destruction. However this sequestered antigen may be released
2. Antigenic variation - Rhinosporidial spores
express varying antigens thereby confusing the whole immune system of
3. Immune suppression - ? possible release of
immuno suppressor agents
4. Immune distraction - Studies of immune cell
infiltration pattern have shown that immune cell infiltration has
occurred in areas where there are no spores, suggesting that these
infiltrates reached the area in response to free antigen released by
the spores. This serves as a distraction.
5. Immune deviation
6. Binding of host immunoglobins
Surgery is the treatment of choice.
Rhinosporidial mass can be removed intranasally, the only problem being
bleeding. Post operatively the patient is started on T. Dapsone in dose
of 100 mg / day for a period of 6 months.
- Habitat - Breeds in ponds (highly
theoretical, spores have not been isolated from ponds even on intense
- Lifecycle - In the absence of viable ways to
culture the organism the life cycle remains highly speculative
- Pathogenicity - does not fullfill any of the
4 criterial laid down by Koch regarding the infectivity
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