From Cat
A mature sporangium of Rhinospordium seeberi is discharging some of its endospores to surface of the skin. A small portion of an immature sporangium is at the edge. It contains only floccular eosinophilic material. 20X

Historically, Rhinosporidium seeberi has been considered to be a fungal organism. However, recent phylogenetic data indicate that it is a protist parasite most closely related to parasites of fish and amphibians[1].

Rhinosporidium infections are characterized by tumor-like mass lesions of the nasal or conjunctival mucosa. Both domestic animals and humans contract the organism from contaminated waters and there is no evidence for direct zoonotic transmission of the organism[2].

Rhinosporidiosis is endemic to India and Sri Lanka, although cases have been reported in Africa, the Americas, and Europe. Most affected patients have a history of temporary or permanent residence within rhinosporidiosis-endemic areas. Rhinosporidiosis is predominantly a human disease; however, it has been documented in many other species, including cats[3].

Clinical signs

Because the typical location of R. seeberi–associated lesions in all species is the nasal mucosa, drinking from contaminated water is likely the source of infection, possibly through superficial wounds in the mucosa. In addition, for ocular disease, dust particles are possible fomites for endospores. Rhinosporidiosis commonly causes single or multiple, sessile or pedunculated, papillomatous, polypoidal or compact masses within the nasal mucosa or, less frequently, the ocular mucosa. These masses are painless, slow-growing, and noninfiltrating. The clinical presentation is thus protracted sneezing and epistaxis associated with a polypoid lesion in the right nostril[4].


Light microscopic examination is required for an accurate diagnosis. This usually reveals a polypoid lesion with numerous sporangia containing maturing endospores. Free endospores were present in the stroma of the polyp and lumen of the nasal cavity. Transmission electron microscopy revealed ultrastructural features typical of Rhinosporidium seeberi. The case was followed clinically for a total of 70 months and there were five attempts at surgical excision[5].

PCR analysis is usually required for definitive diagnosis and to exclude other fungal causes[6][7].

Differential diagnosis

Potential differential diagnoses that should be considered include:


In cats, lesions have been found to recur commonly after surgery, possibly because of incomplete excision or intraoperative contamination of adjacent surfaces with endospores. To prevent recurrence, electrocauterization at the site of excision is recommended. Pharmacologic treatment has not been successful, probably because of the impenetrability of the sporangial wall[9].


  1. 97-98 WSC conference proceedings
  2. Winsconsin Veterinary Medicine Dept
  3. Arseculeratne SN, Mendoza L. Rhinosporidiosis (2005) In: Merz WG, Hay RJ, editors. Topley and Wilson’s microbiology and microbial infections. 10th ed. London: Hodder Arnold; p. 436–75.
  4. Gaines JJ, Clay JR, Chandler FW, Powell ME, Sheffield PA, Keller III AP (1996) Rhinosporidiosis: three domestic cases. Southern Medical Journal 89(1):65-67
  5. Wallin, LL et al (2001) Rhinosporidiosis in a domestic cat. Medical Mycology 39(1):139-141
  6. Herr, RA (1999) Phylogenetic Analysis of Rhinosporidium seeberi's 18S Small-Subunit Ribosomal DNA Groups This Pathogen among Members of the Protoctistan Mesomycetozoa Clade Journal of Clinical Microbiology 37(9):2750-2754
  7. Herr, L et al (1999) Immunolocalization of an endogenous antigenic material of Rhinosporidium seeberi expressed only during mature sporangial development, FEMS Immunology and Medical Microbiology 23:205-212
  8. Gardiner C, Fayer R, Dubey J (1988) An atlas of protozoan parasites in animal tissues. Washington: Armed Forces Institute of Pathology
  9. Fredricks, D.N. et al (2000) Rhinosporidium seeberi: a human pathogen from a novel group of aquatic protistan parasites. Emerg. Infect. Dis. 6:273-282.