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Figure 1.
Left lower palpebral conjunctival polyps. A, Pedunculated lesions with white sporangia (arrows) on the surface. B, Medium-sized encapsulated lesions with central nuclear elements (single arrow) and larger sporangia with spore organisms (double arrow) (hematoxylin-eosin, original magnification ×4). C, Spores spilling out of large sporangia (Gomori methenamine silver stain, original magnification ×40). D, Medium-sized sporangia of the second biopsy specimen (periodic acid–Schiff, original magnification ×10).

Left lower palpebral conjunctival polyps. A, Pedunculated lesions with white sporangia (arrows) on the surface. B, Medium-sized encapsulated lesions with central nuclear elements (single arrow) and larger sporangia with spore organisms (double arrow) (hematoxylin-eosin, original magnification ×4). C, Spores spilling out of large sporangia (Gomori methenamine silver stain, original magnification ×40). D, Medium-sized sporangia of the second biopsy specimen (periodic acid–Schiff, original magnification ×10).

Figure 2.
Transmission electron microscopy and polymerase chain reaction analysis of a polyp. A, Medium-sized sporangia with numerous lipidlike globules (arrow) (original magnification ×1200). B, Cell wall of sporangia with filamentous structures (original magnification ×21 000). C, Polymerase chain reaction analysis of polyp tissue. The first lane shows the molecular markers. The second lane (−) is the negative control in which no tissue was added to the polymerase chain reaction. The third lane (+) shows that a positive polymerase chain reaction product is amplified with the Rhinosporidium seeberi primers from the polyp tissue.

Transmission electron microscopy and polymerase chain reaction analysis of a polyp. A, Medium-sized sporangia with numerous lipidlike globules (arrow) (original magnification ×1200). B, Cell wall of sporangia with filamentous structures (original magnification ×21 000). C, Polymerase chain reaction analysis of polyp tissue. The first lane shows the molecular markers. The second lane (−) is the negative control in which no tissue was added to the polymerase chain reaction. The third lane (+) shows that a positive polymerase chain reaction product is amplified with the Rhinosporidium seeberi primers from the polyp tissue.

1.
Arseculeratne  SN Recent advances in rhinosporidiosis and Rhinosporidium seeberiIndian J Med Microbiol 2002;20 (3) 119- 131
PubMed
2.
Reidy  JJSudesh  SKlafter  ABOlivia  C Infection of the conjunctiva by Rhinosporidium seeberiSurv Ophthalmol 1997;41 (5) 409- 413
PubMedArticle
3.
De Doncker  RMLDe Keizer  RJWOosterhuis  JAMaes  A Scleral melting in a patient with conjunctival rhinosporidiosis. Br J Ophthalmol 1990;74 (10) 635- 637
PubMedArticle
4.
Job  AVenkateswaran  SMathan  MKrishnaswami  HRaman  R Medical therapy of rhinosporidiosis with dapsone. J Laryngol Otol 1993;107 (9) 809- 812
PubMedArticle
5.
Fredricks  DNJolley  JALepp  PWKosek  JCRelman  DA Rhinosporidium seeberi: a human pathogen from a novel group of aquatic protistan parasites. Emerg Infect Dis 2000;6 (3) 273- 282
PubMedArticle
6.
Silva  VPereira  CNAjello  LMendoza  L Molecular evidence for multiple host-specific strains in genus RhinosporidiumJ Clin Microbiol 2005;43 (4) 1865- 1868
PubMedArticle
Research Letters
August 2009

Ocular Rhinosporidiosis Presenting as Chronic Follicular Conjunctivitis in a Contact Lens Wearer

Arch Ophthalmol. 2009;127(8):1076-1077. doi:10.1001/archophthalmol.2009.179

Rhinosporidiosis is a rare granulomatous disease of the mucosal membranes of the eye and nose caused by Rhinosporidium seeberi. Although commonly found in southern India and Sri Lanka, it is rare in North America.1 We report a case of chronic follicular conjunctivitis diagnosed by histopathological analysis, transmission electron microscopy, and polymerase chain reaction analysis to be ocular rhinosporidiosis in a young contact lens wearer from Louisiana.

Report of a Case

A healthy 15-year-old boy from Louisiana had chronic irritation in his left eye without discharge. His social history was remarkable for recent, frequent swimming in a bayou while wearing daily disposable contact lenses. His best-corrected visual acuity was 20/20 OU. Examination revealed a follicular conjunctivitis bilaterally. On his left palpebral conjunctiva, there were numerous pedunculated lesions with white spots on their surfaces (Figure 1A). Otherwise, his examination results were unremarkable. His contact lenses were unavailable for examination. Excisional biopsy of these lesions showed a chronic inflammatory infiltrate with circular periodic acid–Schiff–positive encapsulated lesions (Figure 1B-D) of varying sizes with central nuclear elements or spores, consistent with rhinosporidiosis. The patient stopped his contact lens wear, but the lesions recurred in his left conjunctiva in 11 months. Otolaryngological examination revealed no nasopharyngeal involvement. Another excisional biopsy of the left conjunctival lesions with cryotherapy of the excised margins and an incisional biopsy of the right palpebral conjunctiva were performed. Only the left conjunctiva showed encapsulated lesions. Conjunctival cultures were negative. Transmission electron microscopy of the medium-sized sporangia (Figure 2A) showed a cell wall with radiating filaments (Figure 2B) encapsulating globules of lipidlike material (Figure 2A) around a single nucleus. Polymerase chain reaction analysis of the tissue with genus-specific R seeberi primers correctly amplified a 400–base pair product (Figure 2C). The lesions recurred in the left eye after 3 months, and another biopsy revealed R seeberi.

Comment

First described as a fungal entity, R seeberi is now classified in its own class, Mesomycetozoea.1 It undergoes a life cycle from trophocyte to mature sporangium, which produces endospores that are the infective units. Spores are transmitted from contaminated water and dust1 through epithelial defects on mucosal surfaces. The patient's use of soft contact lenses while swimming likely produced epithelial defects for transmission. Infection causes formation of highly vascular polyps most commonly found in the nasal mucosa and the conjunctiva. Ocular involvement occurs in 15% of cases,2 mostly in the conjunctiva, but dacryocystitis and scleral melting3 have been reported. Involvement of other mucosal membranes, skin, and internal organs has been reported.2 The polyps are covered with white spherules representing the sporangia, described as resembling a strawberry. In this patient the follicular conjunctivitis developed after exposure to the bayou water, and the presence of these strawberry lesions differentiated his condition from other inflammatory conditions such as giant papillary conjunctivitis commonly seen in contact lens wearers. Histopathologically, there is a fibromyxomatous stroma containing trophocytes and sporangia in all stages of development. Treatment involves excision with cryotherapy, but recurrences are common and medical therapy such as with dapsone4 remains controversial. In this patient, the follicular conjunctivitis recurred despite cessation of contact lens wear, also differentiating this condition from other contact lens–related inflammation. Culturing specimens usually does not yield growth of this organism and histopathological analysis has been the mainstay of diagnosis. This report shows identification with histopathological analysis, transmission electron microscopy, and polymerase chain reaction analysis. Interestingly, sequence data of polymerase chain reaction from this organism showed this isolate to be more similar to R seeberi from a canine sample than that of other human isolates.5,6 This patient did not have any dogs at home. As such, these data suggest that the genus Rhinosporidium may possess isolates capable of infecting multiple host types.

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Article Information

Correspondence: Dr Suh, Cornea and External Diseases, Bascom Palmer Eye Institute, University of Miami School of Medicine, 900 NW 17th St, Miami, FL 33136 (lsuh@med.miami.edu).

Financial Disclosure: None reported.

References
1.
Arseculeratne  SN Recent advances in rhinosporidiosis and Rhinosporidium seeberiIndian J Med Microbiol 2002;20 (3) 119- 131
PubMed
2.
Reidy  JJSudesh  SKlafter  ABOlivia  C Infection of the conjunctiva by Rhinosporidium seeberiSurv Ophthalmol 1997;41 (5) 409- 413
PubMedArticle
3.
De Doncker  RMLDe Keizer  RJWOosterhuis  JAMaes  A Scleral melting in a patient with conjunctival rhinosporidiosis. Br J Ophthalmol 1990;74 (10) 635- 637
PubMedArticle
4.
Job  AVenkateswaran  SMathan  MKrishnaswami  HRaman  R Medical therapy of rhinosporidiosis with dapsone. J Laryngol Otol 1993;107 (9) 809- 812
PubMedArticle
5.
Fredricks  DNJolley  JALepp  PWKosek  JCRelman  DA Rhinosporidium seeberi: a human pathogen from a novel group of aquatic protistan parasites. Emerg Infect Dis 2000;6 (3) 273- 282
PubMedArticle
6.
Silva  VPereira  CNAjello  LMendoza  L Molecular evidence for multiple host-specific strains in genus RhinosporidiumJ Clin Microbiol 2005;43 (4) 1865- 1868
PubMedArticle
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