Case Report: Rhinosporidiosis Literature Review.

Rhinosporidiosis is caused by Rhinosporidium seeberi, a pathogen currently considered a fungus-like parasite of the eukaryotic group Mesomycetozoea. It is usually a benign condition, with slow growth of polypoid lesions, with involvement of the nose, nasopharynx, or eyes. The clinical characteristics of a painless, friable, polypoid mass, usually unilateral, can guide the diagnosis, but the gold standard for diagnosis is histopathological findings. This article reviews the epidemiology, pathobiology, clinical manifestations, diagnostic strategies, and treatment approach for rhinosporidiosis.

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

One hundred forty-three cases of rhinosporidiosis, confirmed by smear or biopsy, treated in two major General Hospitals in Sri Lanka over a 14 year period (1995-2009) were analyzed in regard to their epidemiological, clinical, clinicopathological, immunological and microbiological features. Regional variations in incidence, age and sex distribution, bathing history, and histopathology were seen. Lacustrine waters were the commonest probable source of infection (84%). Rivers were a source of Rhinosporidium seeberi in Sri Lanka (11%) and domestic well water was a probable source in 5%. The epidemiological features, clinical presentations and histopathology were similar to those in other series. The antirhinosporidial antibody (mean) titers were IgM--142.1 and IgG--178.5, compatible with rhinosporidiosis of long duration. Mantoux positivity to PPD was found in 65% of normal Sri Lankans, by only 35% of patients with rhinosporidiosis. No outbreaks have been reported in Sri Lanka or India. No animal cases of rhinosporidiosis have been reported in Sri Lanka, although rhinosporidiosis in animals has been repeatedly documented in India.

Cell-mediated immune responses (CMIR) in human rhinosporidiosis.

Cell mediated immune responses (CMIR) to Rhinosporidium seeberi in human patients with rhinosporidiosis have been studied. With immuno-histochemistry, the cell infiltration patterns in rhinosporidial tissues from 7 patients were similar. The mixed cell infiltrate consisted of many plasma cells, fewer CD68+ macrophages, a population of CD3+ T lymphocytes, and CD56/57+ NK lymphocytes which were positive for CD3 as well. CD4+ T helper cells were scarce. CD8+ suppressor/cytotoxic-cytolytic cells were numerous. Most of the CD8+ cells were TIA1+ and therefore of the cytotoxic subtype. CD8+ T cells were not sub-typed according to their cytokine profile; 1L2, IFN-gamma (Tcl); IL4, ILS (Tc2). In lympho-proliferative response (LPR) assays in vitro, lymphocytes from rhinosporidial patients showed stimulatory responses to Con A but lymphocytes from some patients showed significantly diminished responses to rhinosporidial extracts as compared with unstimulated cells or cells stimulated by Con A, indicating suppressor immune responses in rhinosporidiosis. The overall stimulatory responses with Con A suggested that the rhinosporidial lymphocytes were not non-specifically anergic although comparisons of depressed LPR of rhinosporidial lymphocytes from individual patients, to rhinosporidial antigen with those to Con A, did not reveal a clear indication as to whether the depression was antigen specific or non-specific. The intensity of depression of the LPR in rhinosporidial patients bore no relation to the site, duration, or the number of lesions or whether the disease was localized or disseminated. Rhinosporidial extracts showed stimulatory activity on normal control lymphocytes, perhaps indicating mitogenic activity. These results indicate that CMIR develops in human rhinosporidiosis, while suppressed responses are also induced.