Format

Send to

Choose Destination
Curr Opin Infect Dis. 2005 Apr;18(2):113-8.

Rhinosporidiosis: what is the cause?

Author information

1
Department of Microbiology, Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka.

Abstract

PURPOSE OF REVIEW:

Significant advances in knowledge on rhinosporidiosis and Rhinosporidium seeberi were made in 1999, 2000, 2003 and 2004. These advances are reviewed on account of the continuing sporadic occurrence of the disease universally, and because of the availability of new approaches that could resolve persisting enigmas of both the disease and its causative pathogen.

RECENT FINDINGS:

R. seeberi, the pathogen that causes rhinosporidiosis, has been definitively classified using molecular biological tools in a new clade - the Mesomycetozoea, along with 10 parasitic and saprobic microbes. The controversial spherical bodies of the endospores have been shown to comprise both lipid/protein nutritive bodies and other spherical bodies that are metabolizing units that reduce MTT (3-[4,5-dimethyl-2-thiazolyl]-2,5-diphenyl-2H-tetrazolium bromide). This indicates the viability of these spherical bodies, provisionally identified as the electron dense bodies that have also been shown to contain nucleic acids. MTT reduction as an indicator of viability has been used to determine the sensitivity of rhinosporidial endospores to biocides, antimicrobial drugs, and to specific antibodies. Genetic heterogeneity has been identified in strains from humans and animals. Cell-mediated and humoral immune responses have been demonstrated in human patients and in mice. Several mechanisms of immune evasion by R. seeberi have been identified.

SUMMARY:

These findings are applicable in both clinical and laboratory practice, while the basic advances have implications in further work on experimental pathogenicity, the biology of R. seeberi, and on the epidemiology and pathogenesis of rhinosporidiosis.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center