SAMJ VOL. 72 1 AUGUST 1987 Rhinosporidiosis at King Edward VIII

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SAMJ VOL. 72 1 AUGUST 1987 217 Rhinosporidiosis at King Edward VIII Hospital, Durban - 1976 - 1985 A report of 6 cases R. CHETTY, K. COOPER Summary Six cases of the fungal infection, rhinosporidiosis, are documented. Clinical, light microscopic and electron microscopic features of the causative organism (Rhinosporidium seeben) are presented. S Atr Med J 1987; 72: 217·218. Rhinosporidiosis, at one time thought to be in the exclusive domain of the Asian subcontinent, has since been described ubiquitously. It has, however, to our knowledge not been documented in South Africa over the last 20 years. It occurs sporadically in man, horses and cows, but the source of infection is unknown nor has the causative organism, Rhino- sporidium seeberi been conclusively culrured. Rhinosporidiosis is a chronic polyp-inducing infection of the submucous tissue of the nose, eyes, ears and larynx, and occasionally of the genitalia and skin. l The life cycle of Rhino- sporidium begins with a trophocyte stage which has early, intermediate and late phases. The cycle then passes on to pre- and post-cleavage sporangial formation. As the sporangium marures, it becomes fIlled with sporoblasts (endospores). The sporoblasts, which contain spherules, are released into the tissue by ruprure of the sporangia, and go on to become trophocytes. The clinicopathological data and electron microscopic find- ings in 6 cases are described. Patients and methods The patients in this study covering the years 1976 - 1985 ranged from 9 to 15 years in age; all were black, 4 were boys and 2 girls. The conjunctiva was involved in 4 cases and the nostril in 2. The conjunctival lesions were all described as 'granulomatous', with polypoid projections, and clinical diagnoses varied from pyogenic granulomas to viral warts. Both the nasal infections presented as polyps. All lesions were treated by surgical excision and only I recurred. All specimens were formalin fixed. Portions were taken from the paraffin-embedded blocks for electron microscopy. Routine haematoxylin and eosin staining, together with periodic acid-Schiff, mucicannine, Brown Hopps and Giemsa staining, were performed. Fluorescence examination was conducted using unstained sections of paraffin-embedded tissue. Department of Anatomical Pathology, University of Natal and King Edward VIII Hospital, Durban R. CHETTY, M.B. B.CH. (N.V. IREL.) K. COOPER, M.B. CH.B., F.F.PATH.(S.A.) Light microscopy All tissue examined contained the typical organisms of R. seeberi (Fig. 1). An accompanying inflammatory response of lymphocyres, plasma cells and occasiomil eosinophils was seen, and foreign- body-type giant cells and micro-abscesses were also noted. Characteristically, the various morphological forms of the different stages in the life cycle were easily identified. 2 In all lesions ruptured sporangia discharging sporoblasts into the tissue were noted (Fig. 2). Under the light microscope, trophocyres and sporangia were easily detected and appeared as large cystic structures. Fig. 1. Organisms of rhinosporidiosis appearing as cystic struc- tures with a mixed inflammatory reaction. Fig. 2. Ruptured sporangium discharging sporoblasts (endo- spores) into the tissues.

Transcript of SAMJ VOL. 72 1 AUGUST 1987 Rhinosporidiosis at King Edward VIII

SAMJ VOL. 72 1 AUGUST 1987 217

Rhinosporidiosis at King Edward VIIIHospital, Durban - 1976 - 1985A report of 6 cases

R. CHETTY, K. COOPER

Summary

Six cases of the fungal infection, rhinosporidiosis,are documented. Clinical, light microscopic andelectron microscopic features of the causativeorganism (Rhinosporidium seeben) are presented.

S Atr Med J 1987; 72: 217·218.

Rhinosporidiosis, at one time thought to be in the exclusivedomain of the Asian subcontinent, has since been describedubiquitously. It has, however, to our knowledge not beendocumented in South Africa over the last 20 years. It occurssporadically in man, horses and cows, but the source ofinfection is unknown nor has the causative organism, Rhino­sporidium seeberi been conclusively culrured.

Rhinosporidiosis is a chronic polyp-inducing infection ofthe submucous tissue of the nose, eyes, ears and larynx, andoccasionally of the genitalia and skin. l The life cycle of Rhino­sporidium begins with a trophocyte stage which has early,intermediate and late phases. The cycle then passes on to pre­and post-cleavage sporangial formation. As the sporangiummarures, it becomes fIlled with sporoblasts (endospores). Thesporoblasts, which contain spherules, are released into thetissue by ruprure of the sporangia, and go on to becometrophocytes.

The clinicopathological data and electron microscopic find­ings in 6 cases are described.

Patients and methods

The patients in this study covering the years 1976 - 1985 rangedfrom 9 to 15 years in age; all were black, 4 were boys and 2 girls.The conjunctiva was involved in 4 cases and the nostril in 2. Theconjunctival lesions were all described as 'granulomatous', withpolypoid projections, and clinical diagnoses varied from pyogenicgranulomas to viral warts. Both the nasal infections presented aspolyps. All lesions were treated by surgical excision and only Irecurred.

All specimens were formalin fixed. Portions were taken fromthe paraffin-embedded blocks for electron microscopy. Routinehaematoxylin and eosin staining, together with periodic acid-Schiff,mucicannine, Brown Hopps and Giemsa staining, were performed.Fluorescence examination was conducted using unstained sectionsof paraffin-embedded tissue.

Department of Anatomical Pathology, University of Nataland King Edward VIII Hospital, DurbanR. CHETTY, M.B. B.CH. (N.V. IREL.)

K. COOPER, M.B. CH.B., F.F.PATH.(S.A.)

Light microscopyAll tissue examined contained the typical organisms of R. seeberi

(Fig. 1). An accompanying inflammatory response of lymphocyres,plasma cells and occasiomil eosinophils was seen, and foreign­body-type giant cells and micro-abscesses were also noted.Characteristically, the various morphological forms of the differentstages in the life cycle were easily identified.2 In all lesionsruptured sporangia discharging sporoblasts into the tissue werenoted (Fig. 2). Under the light microscope, trophocyres andsporangia were easily detected and appeared as large cysticstructures.

Fig. 1. Organisms of rhinosporidiosis appearing as cystic struc­tures with a mixed inflammatory reaction.

Fig. 2. Ruptured sporangium discharging sporoblasts (endo­spores) into the tissues.

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Electron microscopyUltrastructural examination concurred with the study undenaken

by Kannan-Kutty.3 The trophocyte, the initial stage in thedevelopment of the sporangium, was bi-layered. The inner compo­nent was a pale electron-dense layer which blended imperceptiblywith the outer layer. The latter was made up of a tangle of tubularstructures running in a somewhat haphazard fashion (Fig. 3).Early trophocytes contained lipid bodies together with vesiculatedstructures. As the cycle passed on to the pre-cleavage sporangium,the mature trophocyte, (Fig. 4) was characterised by laminatedbodies (Fig. 5). These consisted of two or more concentricelectron-dense finely granular structures which give rise to sporo­blasts.4

Fig. 3. Wall of trophocyte showing bi-Iayering; the innercomponent being pale and electron dense. The outer layer ismade up of a myriad of tubular structures.

Fig. 4. A mature trophocyte containing laminated bodies.

The sporangia were ftlled with sporoblasts, which were releasedinto the tissue. Mature sporoblasts were uninucleated and theircytoplasm bore multiple vesiculations. The sporoblasts containedspherules. The outer rwo layers of the sporangial cell wall were thesame as those seen in the trophocyte. An additional third layerappeared as an electron-lucent zone.

Fig. 5. Laminated body on extreme right. Other structures aresporoblasts.

AutofluorescenceUltraviolet light revealed fluorescence of the inner sporangial

layer and of the capsules of the sporoblasts in unstained sections.

Discussion

With the advent of electron microscopic studies, rhino­sporidiosis is no longer the enigmatic disease it was. The workof Kannan-Kuny and Teh4 has revealed much about the life­cycle of the organism. Despite inability to culture R. seebericonclusively, Savin02 has concluded that ultrastructurally andhistochemically it is a fungus. Although water has beensuggested as a source, the precise mode of infection is unknown.In this series, the conjunctiva was the more common site ofinvolvement (4 cases). This is contrary to the findings ofSavin02 and Karunaratne,5 both of whom state that nasallesions are commoner.

Of interest also is the fact that all the patients in this serieswere children, the oldest being 15 years. Despite Kannan­Kuny and Teh4 suggesting that drug therapy may be effectivein the endosporulation stage, the popular (and probably mosteffective) mode of treatment is adequate surgical excision.Incomplete removal carries the risk of recurrence.

We wish to thank Dr A. D. Naran, Dr V. Chrystal and Mrs S.Govender.

REFERENCES

1. Cruickshank R, Duguid JP, Swain RHA. Medical Microbiology.' A Guide wthe Laborawry Diagnosis and Control of Infection. 11 rh ed. Edinburgh:Churchill-Livingstone, 1965: 528.

2. Savino DF. Conjunctival rhinosporidiosis - light and electron microscopicstudy. Ophchalmology 1983; 90: 1482-1489.

3. Kannan-Kutty, M. Rhinosporidium seeberi: an electron microscopic study ofits life cycle. Pachology 1974; 6: 63-70. .

4. Kannan-Kutty M, Teh EC. Rhinosporidium seeberi: an ultrastructural studyof its endosporu1ation phase and trophocyte phase. Arch Pachol 1975; 99:51-54

5. Karunaratne WAE. Rhinosporidiosis in Man. London: Athlone Press, 1964:63.