Rhinosporidium seeberi: A Human Pathogen From a Novel Group of Aquatic Protistan Parasites

Disclosures

Emerging Infectious Diseases. 2000;6(3) 

In This Article

Abstract and Introduction

Rhinosporidium seeberi, a microorganism that can infect the mucosal surfaces of humans and animals, has been classified as a fungus on the basis of morphologic and histochemical characteristics. Using consensus polymerase chain reaction (PCR), we amplified a portion of the R. seeberi 18S rRNA gene directly from infected tissue. Analysis of the aligned sequence and inference of phylogenetic relationships showed that R. seeberi is a protist from a novel clade of parasites that infect fish and amphibians. Fluorescence in situ hybridization and R. seeberi-specific PCR showed that this unique 18S rRNA sequence is also present in other tissues infected with R. seeberi. Our data support the R. seeberi phylogeny recently suggested by another group. R. seeberi is not a classic fungus, but rather the first known human pathogen from the DRIPs clade, a novel clade of aquatic protistan parasites (Ichthyosporea).

Rhinosporidiosis manifests as slow-growing, tumorlike masses, usually of the nasal mucosa or ocular conjunctivae of humans and animals. Patients with nasal involvement often have unilateral nasal obstruction or bleeding due to polyp formation. The diagnosis is established by observing the characteristic appearance of the organism in tissue biopsies (Figure 1). Treatment consists of surgical excision, but relapse occurs in approximately 10% of patients[1]; antimicrobial therapy is not effective[2]. Rhinosporidiosis occurs in the Americas, Europe, Africa, and Asia but is most common in the tropics, with the highest prevalence in southern India and Sri Lanka. A survey of schoolchildren from Pallam, India, found 11 cases in 781 children examined (prevalence 1.4%)[3]. Autochthonous cases have been reported from the southeastern United States[4]. Studies have linked infection to swimming or bathing in freshwater ponds, lakes, or rivers[2,5].

Figure 1. Histology of rhinosporidiosis. A formaldehyde-fixed section of human nasal polyp was stained with Periodic acid-Schiff (PAS) and visualized by bright-field microscopy at 400X magnification. The thick walls of immature R. seeberi trophocytes stain with PAS (pink), and the spherical organisms are surrounded by inflammatory cells.*

The etiologic agent of rhinosporidiosis, Rhinosporidium seeberi, is an enigmatic microbe that has been difficult to classify. Recently, R. seeberi has been considered a fungus, but it was originally thought to be a protozoan parasite[2]. Its morphologic characteristics resemble those of Coccidioides immitis: both organisms have mature stages that consist of large, thick-walled, spherical structures containing smaller daughter cells (endospores). In addition, R. seeberi is visualized with fungal stains such as methenamine silver and Periodic acid-Schiff, as well as mucicarmine, which stains the fungus Cryptococcus neoformans. R. seeberi has not been detected in the environment, and its natural host or reservoir is unknown. Attempts to propagate this organism on artificial media have failed, as has continuous cocultivation with human cell lines[6].

We report a molecular approach for establishing the phylogenetic relationships R. seeberi to other eukaryotes. This approach is based on amplification of the small subunit rRNA gene sequence from infected tissue, as in the method used to identify the culture-resistant bacillus of Whipple disease[7]. The sequence of the small subunit rRNA gene has proven to be a useful gauge of evolutionary relationships for many organisms from diverse taxonomic groups[8].

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