Literature DB >> 26015750

Rhinosporidiosis and the pond.

M Prakash1, J Carlton Johnny1.   

Abstract

Rhinosporidiosis is a fungal disease caused by the organism Rhinosporidum seeberi. The life cycle and mode of infection are vague, and there are many hypothesis on it. Its prevalence in the world is unique as it is only limited to certain regions like India, Pakistan and Sri Lanka. We have tried to correlate the various factors, which will probably be associated with this pattern of prevalence of the disease. We have included factors like community practices, climatic conditions, rain fall pattern, water physiochemical properties, zoonotic and the aquatic organism composition in the specified regions. Thus, it serves as a wholesome idea of why the disease must only be prevalent in certain parts of the world.

Entities:  

Keywords:  Pond; Rhinospordium seebri; rhinosporidiosis

Year:  2015        PMID: 26015750      PMCID: PMC4439710          DOI: 10.4103/0975-7406.155804

Source DB:  PubMed          Journal:  J Pharm Bioallied Sci        ISSN: 0975-7406


Rhinosporidiosis is an infection caused by a fungi Rhinosporidium seeberi. It is generally acquired by bathing in ponds contaminated by animal feces, but still there is no proven theory[1] about the complete life cycle of the organism. It usually presents as strawberry like[2] bleeding polyp in the nose and in severe cases as disseminated rhinosporidiosis. Rhinosporidiosis has been reported from about 70 countries[1] with diverse geographical features although the highest incidence has been from India and Sri Lanka.[1] Most cases of human rhinosporidiosis in western temperate and middle eastern countries have occurred in expatriate Indians, who probably acquired the disease in their native lands.[1] This geographic distribution is, usually, related to certain environmental and cultural practices that are confined to these specific regions. So, if we are able to identify the uniqueness of the various factors like community practices, climatic conditions, rain fall pattern, water physiochemical properties, zoonotic and aquatic organism composition in the specified regions from the rest of the world, we can conclude that a hypothesis about the various reasons for the endemicity.

Identification of the Organism

The disease was first described by Seeber in Argentina[3] and it was Ashworth who described the life cycle of R. seeberi and he concluded that the nearest relative of Rhinosporidium are not sporozoa but lower fungi (phycomycetes) such as Chytridineae in which, suborder was near Olpidiaceae.[4] The microsopic view of the organism is seen in the Figure 1[5]. Culture of R. seeberi was described from Trivandrum[6] and from Delhi.[7] Their observation suggests that the rhinosporidiosis is caused by a cyanobacterium – Microcystis sp.[78] Subsequently polymerase chain reaction of the 18S r-RNA gene and sequencing of nearly full length 18S subunit of R. seeberi states that it belongs to clusters with novel group of fish parasites referred to as the Dermocystidium, Rossete agensts, Istiophorus and Psorospermium clade,[1] near the animal fungal divergence.[910]
Figure 1

Rhinospordiosis seebri cysts

Rhinospordiosis seebri cysts

Hypothesized Mode of Spread

Demellow's theory[11] of direct transmission - this theory propounded by Demellow had its acceptance for quite some time. He postulated that the infection always occurred as a result of direct transmission of the organism. When nasal mucosa comes into contact with infected material while bathing in common ponds,[12] infection found its way into the nasal mucosa. Karunaratne[13] accounted for satellite lesions in the skin and conjunctival mucosa as a result of auto inoculation. He 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. Rhinosporidiosis affecting distant sites could be accounted for only through hematogenous spread.[1]

Epidemiology of the Disease

The disease is usually seen in about 70 countries,[1] but highest cases are reported only in India and Sri Lanka.[1] The prevalence is more in the male sex.[12] The peak age of incidence is around the second and third decade. The areas of high incidence are seen in [Figure 2].
Figure 2

Areas of high incidence

Areas of high incidence

Reasons for Endemicity

Now, let us compare and reason out the various parameters which might be responsible for the distribution of the disease. For our study comparison, we have taken 3 countries in India, where there is a high incidence of rhinosporidiois; and USA, UK where the incidence is relatively less. Let us consider the various parameters one by one.

Cultural Practices

India is developing the country when compared to USA or the UK. Thus, one of the prime occupations is cattle rearing in the rural areas and also the use of cattle for various other uses like agriculture,[13] dairy products, etc., In rural areas, the most accessible large water body for cleaning the cattle and performing other duties that require a large quantity of water like washing clothes, taking bath, etc., is a pond. In support of this, it is seen that the most of the villages have their temple pond called “Thepakulam” for performing religious activities. The other use of the ponds is that it is used as a reservoir of water as these are draft prone areas, and it can be used for small scale fishing for the local inhabitants. These factors are usually not seen in the western countries, which makes it highly impossible for the transmission of the disease. It is common in these areas for the men to do this work and women mostly are home makers thus this may contribute to an increased incidence in males.[12] It is also seen to be more prevalent among Muslims in Sri Lanka due to the mechanical cleaning of the nostril with a finger, during prayer, which may cause mechanical innoculation.[13]

Climatic Conditions

The climatic conditions of both illinois and madurai are given in the [Tables 1 and 2].[1415] It is clearly seen that the temperature in India is relatively high which aids in the spore formation of the fungi when compared to the temperature abroad. Another important factor is the increased humidity in the tropical diseases creating a good environment for spore formation. The rain fall pattern also is widely variable in these regions.
Table 1

Climatic condition in Illinois USA

Table 2

Climate condition in madurai

Climatic condition in Illinois USA Climate condition in madurai

Physiochemical Properties of Water

The physiochemical properties of water from three regions are given in the [Tables 3–5].[161718] When we compare the most important factors like pH, sodium, potassium, chloride, alkalinity, we find that there are gross variations in them.
Table 3

Physiochemical properties of water in kanyakumari

Table 5

Physiochemical properties of water in Alabama (USA)

Physiochemical properties of water in kanyakumari Physiochemical properties of water in West London (UK) Physiochemical properties of water in Alabama (USA) PH in India is more acidic when compared to the other countries. Sodium content in India is very less when compared to the other states. Whereas the chloride content in India is very less when compared to the USA, UK. It is a known fact that the chlorine is a potent inhibitor of microorganism growth.

Misclaneous Causes

It is seen that incidence of rhinosporidiosis is more common in “O” blood group individual (about 70%). In India, the highest incidence of rhinosporidiosis was in Group O (70%) though in the population Groups A, B, and O are distributed “fairly equally”. The next highest incidence was in Group AB though in the general population Group AB is rare. Jain in India reported that the blood group distribution was too variable to draw any conclusion.[19] Another major factor can be the bio diversity of the ponds that are different in these regions. There have not been exact documented referenced between the symbiosis between rhinosporidiosis and other organisms, but it is hypothized by many. This aspect is an area of future research. It may also be postulated that the genetic makeup and human leukocyte antigen type of the people in the endemic areas may be different when compared to the others. This must always be kept in the back of our mind. But still there has not yet been any major attempt to prove this, but this might be an area of potential research in the future.[20]

Conclusion

Thus on consolidating all the parameters we can arrive at a hypothesis that the climatic conditions, physiochemical properties of water in India, Sri Lanka are more in favor of the fungal growth when compared to the west. It is essential for any fungi to require humidity and a warm temperature for its sporulation. So these tropical regions are very good breeding grounds for the fungi. The most important of all factors is the cultural habits which lead to the spread of the disease. It is not customary in the west to clean cattle in local ponds or even take bath along with the cattle in the pond. Thus there is still more research needed to establish more strong correlation factors between the pond and rhinosporidiosis.
Table 4

Physiochemical properties of water in West London (UK)

  9 in total

1.  Patterns of rhinosporidiosis in Sri Lanka: comparison with international data.

Authors:  S N Arseculeratne; S Sumathipala; N B Eriyagama
Journal:  Southeast Asian J Trop Med Public Health       Date:  2010-01       Impact factor: 0.267

2.  Management of rhinosporidiosis-newer concept.

Authors:  H K Jviarfatia; M V Kirtane
Journal:  Indian J Otolaryngol Head Neck Surg       Date:  1997-01

3.  Phylogenetic analysis of Rhinosporidium seeberi's 18S small-subunit ribosomal DNA groups this pathogen among members of the protoctistan Mesomycetozoa clade.

Authors:  R A Herr; L Ajello; J W Taylor; S N Arseculeratne; L Mendoza
Journal:  J Clin Microbiol       Date:  1999-09       Impact factor: 5.948

4.  Rhinosporidiosis: a study that resolves etiologic controversies.

Authors:  K B Ahluwalia; N Maheshwari; R C Deka
Journal:  Am J Rhinol       Date:  1997 Nov-Dec

5.  Culture of the organism that causes rhinosporidiosis.

Authors:  K B Ahluwalia
Journal:  J Laryngol Otol       Date:  1999-06       Impact factor: 1.469

6.  Culture of Rhinosporidium seeberi: preliminary report.

Authors:  S Krishnamoorthy; V P Sreedharan; P Koshy; S Kumar; C K Anilakumari
Journal:  J Laryngol Otol       Date:  1989-02       Impact factor: 1.469

7.  Recent advances in rhinosporidiosis and Rhinosporidium seeberi.

Authors:  S N Arseculeratne
Journal:  Indian J Med Microbiol       Date:  2002 Jul-Sep       Impact factor: 0.985

8.  A molecular approach (multiplex polymerase chain reaction) for diagnosis of rhinosporidiosis.

Authors:  Somnath Saha; Dibyakanti Mondal; Dimple Khetawat; Atanu Roy; Sekhar Chakrabarti; Basudev Bhattacharya
Journal:  Indian J Otolaryngol Head Neck Surg       Date:  2002-10

9.  Rhinosporidium seeberi: a human pathogen from a novel group of aquatic protistan parasites.

Authors:  D N Fredricks; J A Jolley; P W Lepp; J C Kosek; D A Relman
Journal:  Emerg Infect Dis       Date:  2000 May-Jun       Impact factor: 6.883

  9 in total
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1.  External dacryocystorhinostomy for isolated lacrimal sac rhinosporidiosis - A suitable alternative to dacryocystectomy.

Authors:  Nandini Bothra; Suryasnata Rath; Ruchi Mittal; Devjyoti Tripathy
Journal:  Indian J Ophthalmol       Date:  2019-05       Impact factor: 1.848

2.  A case of primary disseminated rhinosporidiosis and dapsone-induced autoimmune hemolytic anemia: A therapeutic misadventure.

Authors:  Ritwik Ghosh; Subhargha Mondal; Dipayan Roy; Adrija Ray; Arpan Mandal; Julián Benito-León
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