Rhinosporidiosis is a benign chronic granulomatous infection caused by Rhinosporidiosis seeberi (R. seeberi). Rhinosporidiosis is endemic in South Asia, notably in Southern India and Sri Lanka. The common sites of involvement are the nose and nasopharynx followed by ocular tissue. Rhinosporidiosis is also known to involve many rare sites and may become disseminated to ocular in generalized form. Rhinosporidiosis of parotid duct is extremely rare. The case presented here is of 18-year-old male from the nonendemic zone of Nepal with a proliferative mass in the parotid duct. Although rhinosporidiosis was not taken into consideration in the clinical differential diagnosis, eventual histopathological diagnosis confirmed rhinosporidiosis. Thus clinicians should be flexible in the differential diagnosis of proliferative growth in the parotid duct, even in those cases which are from nonendemic areas. 1. Introduction Rhinosporidiosis is a benign chronic granulomatous disease caused by Rhinosporidium seeberi (R. seeberi) [1]. It occurs sporadically and is known to be noncontagious. Although human rhinosporidiosis occurs universally with higher occurrence in parts of South Asia, it is endemic, especially in Southern India and Sri Lanka [2–4]. The most common site of infection in humans is the nose [1]. Other sites include the nasopharynx, larynx, oropharynx, conjunctiva, lacrimal sac, and genital mucosa. Intraorally, rhinosporidiosis is known to involve the lip, palate, and uvula, secondarily, by direct extension from nasal and nasopharyngeal lesions [1]. Primary involvement of the parotid duct is extremely rare. We present a case of 18-year-old male from nonendemic zone of Nepal with proliferative mass in the parotid duct and recalcitrant to conventional management that subsequently showed the presence of R. seeberi on histopathologic analysis of the specimen. 2. Case Report An 18-year-old male reported to the oral and maxillofacial department with complaints of swelling on left side of the face since 10 days, associated with a history of an increase in its size and also pain associated with swelling during meal time. No other associated symptoms were reported. There was no history of trauma in the recent past. Patient had history of consumption of unprocessed well water. On clinical examination, patient was moderately built with no signs of parlor, jaundice, or lymphadenopathy. Systemic examination also did not reveal any abnormalities. The nose, nasopharynx, oropharynx, and eyes appeared normal. On local examination, there was a single, soft to firm
References
[1]
S. N. Jain and P. V. R. Rao, “Rhinosporidiosis,” Current Opinion in Otolaryngology and Head and Neck Surgery, vol. 6, no. 3, pp. 182–185, 1998.
[2]
O. Lupi, S. K. Tyring, and M. R. McGinnis, “Tropical dermatology: fungal tropical diseases,” Journal of the American Academy of Dermatology, vol. 53, no. 6, pp. 931–951, 2005.
[3]
W. A. E. Karunnaratne, Rhinosporidiosis in Man, Athlone Press, London, UK, 1964.
[4]
C. Satyanarayana, “Rhinosporidiosis with a record of 255 cases,” Acta Oto-Laryngologica, vol. 51, pp. 348–366, 1960.
[5]
V. K. Ayyar, “Rhinosporidiosis in cattle, a case recorded in a bullock,” Transactions of the Far-Eastern Association of Tropical Medicine, vol. 3, p. 658, 1927.
[6]
G. R. Seeber, Nenvo exporozoario parasito del hombre: dos casos encontrades en po lipos nasals [M.S. thesis], Universidad Nacional de Buenos Aires, Buenos Aires, Argentina, 1900.
[7]
K. J. Kwon-Chung and J. E. Bennett, “Rhinosporidiosis,” in Medical Mycology, I. C. T. Kwon-Chung and J. E. Bennett, Eds., pp. 695–706, Lea & Febiger, Philadelphia, Pa, USA, 1992.
[8]
J. H. Ashworth, “On Rhinosporidium seeberi with special reference to its sporulation and affinities,” Transactions of the Royal Society of Edinburgh, vol. 53, pp. 301–342, 1923.
[9]
R. A. Herr, L. Ajello, J. W. Taylor, S. N. Arseculeratne, and L. Mendoza, “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, vol. 37, no. 9, pp. 2750–2754, 1999.
[10]
S. L. Kutnick and J. D. Kerth, “Rhinosporidiosis,” Laryngoscope, vol. 86, no. 10, pp. 1579–1583, 1976.
[11]
S. Mahapatra, S. Tripathy, G. Rath, and G. Misra, “Rhinosporidiosis of parotid duct: a rare case report,” Indian Journal of Pathology and Microbiology, vol. 50, no. 2, pp. 320–322, 2007.
[12]
R. G. Topazian, “Rhinosporidiosis of the parotid duct,” British Journal of Oral Surgery, vol. 4, pp. 12–15, 1966.
[13]
S. N. Jain, “Aeitiology and incidence of rhinosporidiosis,” Indian Journal of Otology, vol. 19, p. 1, 1987.
[14]
Z. Vuiovic, A. Bobic-Radovanovic, Z. Latkovic, and Z. Radovanovic, “An epidemiological investigation of the first outbreak of rhinosporidiosis in Europe,” Journal of Tropical Medicine and Hygiene, vol. 98, no. 5, pp. 333–337, 1995.
[15]
C. Ramanan and A. Ghorpade, “Giant cutaneous rhinosporidiosis,” International Journal of Dermatology, vol. 35, no. 6, pp. 441–442, 1996.
[16]
D. M. Thappa, S. Venkatesan, C. S. Sirka, T. J. Jaisankar, G. Gopalkrishnan, and C. Ratnakar, “Disseminated cutaneous rhinosporidiosis,” Journal of Dermatology, vol. 25, no. 8, pp. 527–532, 1998.
[17]
N. R. de Silva, H. Huegel, D. N. Huegel et al., “Cell-mediated immune responses (CMIR) in human rhinosporidiosis,” Mycopathologia, vol. 152, no. 2, pp. 59–68, 2001.
[18]
K. S. Loh, S. M. Chong, Y. T. Pang, and K. Soh, “Rhinosporidiosis: differential diagnosis of a large nasal mass,” Otolaryngology, vol. 124, no. 1, pp. 121–122, 2001.
[19]
B. J. Longley, Fungal Diseases in Lever’s Histopathology of Skin, Lippincott Williams & Wilkins, Philadelphia, Pa, USA, 8th edition, 1997.
[20]
S. N. Arsecularatne, “Recent advances in rhinosporidiosis and rhinosporidium seeberi,” Indian Journal of Medical Microbiology, vol. 20, pp. 119–131, 2002.
