Rhinosporidiosis in the parotid duct: a rare case report.

Endemic to South India and Sri Lanka, Rhinosporidiosis is a chronic granulomatous infection caused by an agent of uncertain taxonomy: Rhinosporidium seeberi. Although it commonly manifests as a proliferative nasal lesion, many cases of Rhinosporidiosis have been reported where it has appeared as an extranasal lesion. The reported extranasal sites include the eye, ear, trachea, and parotid duct. However, the involvement of the parotid duct is quite rare, even among extranasal sites. The case presented is an adult female from the non-endemic zone of East India 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. As this appears to be the second case of Rhinosporidiosis in the parotid duct in East India in 4 years, we encourage clinicians to be flexible in the differential diagnosis of proliferative growth in the parotid duct, even in those from non-endemic areas.

Rhinosporidiosis of parotid duct.

Rhinosporidiosis is a benign chronic granulomatous infection caused by Rhinosporidium seeberi. Rhinosporidiosis is endemic in south Asia, notably in southern India and Sri Lanka. Majority of the cases have been reported to occur in upper respiratory sites, notably anterior nares, nasal cavity, nasopharynx, larynx and soft palate. Only two rare cases of involvement of parotid duct, have been reported in literature. Hence, this case will probably be the third to be reported.

Structural differences between alcoholic and diabetic parotid sialosis.

UNLABELLED: Between the sialosis' etiologic agents, we can find the chronic alcoholism and diabetes. Both nosologic entities are described using a similar histopathologic pattern. OBJECTIVES: The purpose of this work has been analyzing and comparing the histopathological differences between the diabetic and alcoholic sialosis. STUDY DESIGN: We studied 7 parotid glands samples of diabetic patients and 4 samples of normal glands obtained from surgical material were used as a control. For the comparative study, we used 12 parotid glands from chronic alcoholic patients with clinical diagnosis of cirrhosis and 6 autopsies on individuals who had died from alcoholic hepatic cirrhosis. This material was fixed in formaline, processed for embedding in paraffin, standard coloration techniques and immunotechnique for cytokeratin EA/1 y EA/3. RESULTS: In the cases of diabetics, the parotid gland was characterised by the presence of small acini, a bigger number of lipid intracytoplasmic droplets in the acinar and ductal cells, as well as an abundant adipose infiltration in the stroma when compared to the alcoholics. We observed that the cytokeratins' expression was heterogeneous at the acinar level, and very positive in the hyperplasic ducts, compared to the alcoholic and control groups. CONCLUSIONS: These qualitative valorations indicate the differences between the histopathologic pattern of sialosis with different origins.