Rhinosporidium seeberi

Taxobox
color = khaki


image_caption =
regnum = Protista
phylum = Choanozoa
classis = Mesomycetozoea
ordo = Dermocystidium
familia =
genus = Rhinosporidium
species = seeberi
binomial =
binomial_authority =

Rhinosporidium seeberi was first identified in 1892 but was comprehensively described in 1900 by Seeber.

There are many aspects of the disease and of the pathogen "Rhinosporidium seeberi" which remain problematic and enigmatic. These include, the pathogen’s natural habitat, some aspects of its ‘life cycle’, its immunology, some aspects of the epidemiology of the disease in humans and in animals, the reasons for the failure at "in vitro" culture and establishment of disease in experimental animals and hence paucity of information on its sensitivity to drugs, and the immunology of the pathogen.

Incompletely resolved aspects of the disease are its epidemiology and its pathogenesis. (see review refs. 14, 15, 22).

Phylogeny

The taxonomic and evolutionary position of this organism has been unclear until relatively recently. Traditionally it was classified among the fungi. Using DNA sequences it has been found that the closest relatives of this organism are fish parasites in the Kingdom Protoctista. This monophyletic group has been named the Mesomycetozoea and includes "Dermocystidium", the Rosette Agent (a fish pathogen) and "R. seeberi". (see refs. 2, 6, 13).

Epidemiology

Infection with this organism has been reported from ~70 countries with the majority of cases (95%) reported from India and Sri Lanka: per capita Sri Lanka has the highest incidence in the world.

An all India survey conducted in 1957 found that this disease was absent from the states of Jummu & Kashmir, Himachal Pradesh, Punjab, Haryana and the North Eastern states of India. In TamilNadu 4 endemic areas were identified in the survey - (Madurai, Ramnad, Rajapalayam and Sivaganga). The common denominator found in these areas was the practice of bathing in common ponds.

Theories of transmission

1. Demellow's theory of infection 2. Karunarathnae's autoinoculation theory 3. Haematogenous spread - to distant sites 4. Lymphatic spread - causing lymphadenitis (rare)

Demellow postulated that while bathing in common ponds the nasal mucosa came into contact with infected material which the organism invaded. Karunarathnae proposed that the satellite lesions in skin and conjunctival mucosa arose as a result of auto inoculation.

Natural habitat

Karunarathnae also porposed that "Rhinosporidium" existed in a dimorphic state - a saprotroph in soil and water and a yeast form inside living tissues.Recent studies done using Fluoroscent in-situ-hybridization techniques provide evidence that its natural habitat to be reservoir water and perhaps soil contaminated with it. [The Identification of the Natural Habitat of Rhino-sporidium seeberi with R. seeberi-Specific in situHybridization Probes. Kumara Kaluarachchi,Saranga Sumathipala,Navaratne Eriyagama,Dhammika Atapattu,Sarath Arseculeratne .J Infect Dis Antimicrob Agents 2008;25:25-32.]

Pathology

Of interest was the report indicating that patients with rhinosporidiosis possess anti-"R. seeberi" IgG to an inner wall antigen expressed only during the mature sporangial stage. This finding suggests that the mapping of antigenic proteins may lead to important antigens with the potential as vaccine candidates (see ref. 1).

Humoral and Cell-mediated Immune responses in human patients and in experimental mice have been defined; several mechanisms of immune evasion by "R. seeberi" have been identified (see 9, 10, 16)

A novel method for the determination of the viability of rhinosporidial endospores by MTT-reduction (ref. 17) led to the study of the sensitivity of endospores to biocides (ref. 23) and anti-microbial drugs (in preparation for submission).

Clinical features

This organism infects the mucosa of the nasal cavity producing a mass like lesion. This mass appears to be polypoidal in nature with a granular surface speckled with whitish spores. The rhinosporidial mass has been classically described as a strawberry like mulberry mass. This mass may extend from the nasal cavity into the nasopharynx and present itself in the oral cavity. These lesions commonly cause bleeding from the nasal cavity.

"Rhinosporidium seeberi" can also affect the lacrimal gland and also rarely the skin and genitalia.

Common sites affected:

# Nose - 78%
# Nasopharynx - 68%
# Tonsil - 3%
# Eye - 1%
# Skin - very rare

References

Herr R. A. "et al." (1999) Immunolocalization of an endogenous antigenic material of "Rhinosporidium seeberi" expressed only during mature sporangial development. FEMS. Imm. & Med. Micro. 23: 205-212.

Herr R. A. "et al." (1999) Phylogenetic analysis of "Rhinosporidium seeberi"’s 18S small subunit ribosomal DNA groups this pathogen among members of the Protoctistan "Mesomycetozoa" Clade. J. Clin. Micro. (Sept) 2750-2754.

Atapattu D. N. "et al." (1999) Purification of the endospores and sporangia of "Rhinosporidium seeberi" on Percoll columns. Mycopathologia 145: 113-119.

Mendoza L. "et al." (1999) "In vitro" studies on the mechanisms of endospore release by "Rhinosporidium seeberi". Mycopathologia 148: 9-15

Arseculeratne S. N. "et al.", (2000) Failure to infect congenitally immunodeficient mice SCID and nude mice with "Rhinosporidium seeberi". Med. Mycology 38: 393-395

Fredricks D. N., Jolley J. A., Lepps P. W., Kosek J. C. & Relman D. A. (2000) "Rhinosporidium seeberi": a human pathogen from a novel group of aquatic Protistan parasites. Emerging infectious diseases 6(3): 273-282.

Arseculeratne S. N. (2001) "Microcystis aeruginosa" as the cause of rhinosporidiosis . Mycopathologia 151: 3-4.

Mendoza L. "et al." (2001) (reply to K. B. Ahluwalia's ideas on "M. aeruginosa" as the cause of rhinosporidiosis). J. Clin. Micro. 39(1): 413-415.

Sharmini Jayasekera. "et al" (2001) Cell-mediated immune responses to "Rhinosporidium seeberi" in mice, Mycopathologia, 152: 69-79.

de Silva N. R. "et al." (2001) Cell-mediated immune responses in human rhinosporidiosis. Mycopathologia 152: 59-68.

Arseculeratne S. N. "et al." (2001) Lymphadenitis, trans-epidermal elimination and unusual histopathology in human rhinosporidiosis. Mycopathologia 153: 57-69. (This is the first report on lymphadenitis in rhinosporidiosis)

Appuhamy S., Atapattu D. N., Arseculeratne S. N. & Eriyagama N. B. (2002) Strain variation in "Rhinosporidium seeberi" Proc. of the Sri Lanka College of Microbiologists, OP7.

Mendoza L., Taylor J. W. & Ajello L. (2002) The Class Mesomycetozoea: A heterogeneous group of microorganisms at the Animal-Fungal boundary. Annual Rev. Microbiol. 56: 315-344.

Arseculeratne, S. N. & Atapattu, D. N. (2002) Recent advances in knowledge on "Rhinosporidium seeberi" and rhinosporidiosis. In: Fungi in human and animal health. R. K. S. Kushwaha ed., Jodhpur Scientific Publishers, India

Arseculeratne, S. N. (2002) Recent advances in rhinosporidiosis and "Rhinosporidium seeberi". Indian J. Med. Microbiol. 20(3): 119-131.

Arseculeratne, S. N. (2003) Mechanisms of immune evasion by "Rhinosporidium"seeberi. Bulletin of the Sri Lanka College of Microbiologists 1(1): 56-58.

Arseculeratne, S. N. & Atapattu, D. N. (2004) The assessment of the viability of theendospores of Rhinosporidium seeberi with MTT (3- [4, 5-dimethyl-2-thiazolyl] -2, 5diphenyl-2H-tetrazolium bromide). Mycological Research 108(12): 1423-1430.

Arseculeratne S. N., Kumarasiri P. V. R., Rajapakse R. P. V. J., Perera, N. A. N. D. Arseculeratne G., & Atapattu D. N. (2004) Anti-rhinosporidial antibody levels in patients with rhinosporidiosis and in asymptomatic persons in Sri Lanka. Mycopathologia 158: 157-164.

Arseculeratne S. N. (2005) Rhinosporidiosis – What is the cause? Current Opinion In Infectious Diseases 18: 113-118.

Arseculeratne S. N., Atapattu D. N. & Wickramaratne K. (2005) The nature and significance of the electron dense bodies of the endospores of "Rhinosporidium seeberi": their reactions with MTT (3- [4, 5-dimethyl-2-thiazolyl] -2, 5-diphenyl-2H tetrazolium bromide). Med. Mycology 43: 261-273.

Arseculeratne S. N., Atapattu D. N. & Eriyagama N. B. (2005) Human anti rhinosporidial antibody does not cause metabolic inactivation or morphological damage in endopsores of "Rhinosporidium seeberi", "in vitro". Indian J. Med. Microbiol. 23(1): 14-19.

Arseculeratne, S.N. & L. Mendoza. (2005) "Rhinosporidium seeberi". In: Topley & Wilson’s Microbiology & Microbial Infections, 10th ed., vol.5, Medical Mycology, R.J. Hay & W. Merz, vol. Eds., London, Hodder-Arnold

Arseculeratne S. N., Atapattu D. N., Balasooriya, Pushpa & Fernando, R. (2006) The effect of biocides (antiseptics and disinfectants) on the endospores of "Rhinosporidium seeberi". Indian J. Med. Microbiol. (in press)

Kumara Kaluarachchi,Saranga Sumathipala,Navaratne Eriyagama,Dhammika Atapattu,Sarath Arseculeratne (2008). The Identification of the Natural Habitat of Rhino-sporidium seeberi with R. seeberi-Specific in situ Hybridization Probes..J Infect Dis Antimicrob Agents 2008;25:25-32.

External links

* [http://www.geocities.com/rhinosporidiosisseeberi Rhinosporidiosis Research Group]
* [http://www.orlhns.info/index.php?title=Rhinosporidiosis Concise information on Rhinosporidiosis]
* [http://rad.usuhs.edu/medpix/tf_case.html?mode=pt&pt_id=10955#top Rhinosporidium Images]
* [http://www.drtbalu.com/rhinosporidiosis.html drtbalu otolaryngology online]