A vast majority of patients with AIDS present with oral manifestations [1]. The essential risk factors that influence the development of such oral manifestations are the low number of CD4 lymphocytes, xerostomia, and a lack of antiretroviral therapy [2]. The most common oral lesion seen in HIV disease is oropharyngeal candidiasis [1]. Here we present a case of an HIV-positive patient who presented with oral ulcers caused by Rhodotorula mucilaginosa, which to our knowledge has not been reported in the literature. A 45-year-old HIV-positive patient presented to the internist with complaints of non-healing oral ulcers and white patches in the mouth of 2 months' duration associated with painful swallowing and dry mouth. The patient was a known case of HIV for 6 years and his CD4 cell count at presentation was 52 cells/μl. He had been receiving oral fluconazole for 2 months and antiretroviral therapy for 4 years. He was currently on saquinavir, zidovudine and lamivudine. The patient showed no improvement on the current therapy, instead the ulcers increased in size. On examination, the oral ulcers were bilateral, deep, and 1 ×1 cm in size (Fig. 1a). Swabs were obtained from the edges of the ulcers and were subjected to direct Gram staining and culture on Sabouraud's dextrose agar (SDA) and SDA with chloramphenicol in duplicate; they were then incubated at 25°C and 37°C.Fig. 1: Oral ulcer caused by Rhodotorula mucilaginosa.(a) Clinical photograph showing a deep ulcer on the buccal mucosa (arrow). (b) Reddish pink yeast-like creamy colonies of Rhodotorula mucilaginosa on Sabouraud's dextrose agar and (inset) Gram-stained picture of R. mucilaginosa.On direct microscopy large round yeast cells with narrow angle budding and a thin capsule were seen. Reddish pink yeast-like creamy colonies were isolated in pure culture 5 days later on SDA at 25°C and 37°C, which showed large round budding yeast cells and no hyphae (Fig. 1b). The organism did not ferment glucose, sucrose, lactose, galactose, maltose or trehalose. On performing carbohydrate assimilation tests on yeast nitrogen base agar, glucose, sucrose, trehalose, D-xylose, raffinose, and D-arabinose were assimilated, whereas lactose, melibiose, galactose, maltose, cellobiose and inositol were not. Urea was hydrolysed. Repeated sampling showed similar results. Based on the above tests, a diagnosis of R. mucilaginosa (earlier called Rhodotorula rubra) oral ulcers was made. The patient was started on itraconazole thereafter and antiretroviral therapy was continued. A dramatic improvement in the symptoms was noted, with healing of the ulcers. A CD4 cell count was repeated and the count was recorded as 42 cells/μl with no improvement. R. mucilaginosa is a yeast found in air, soil, lakes [3], ocean water [4], and dairy products. It can be found in shower curtains, bath tubs or tooth brushes [5]. On Gram staining it is a Gram-positive yeast and may show a thin capsule on India ink preparation. On SDA, cultures are coral pink, smooth, sometimes reticulate, rugose or corrugated, and moist to mucoid yeast like in appearance. The germ tube test is negative, hydrolysis of urea is positive, growth on cycloheximide medium is negative and growth at 37°C is variable [6]. Rhodotorula differs from Cryptococcus by its inability to assimilate inositol and the carotenoid pigment, and from Candida by producing pink-to-red colonies, lacking pseudohyphae and its inability to ferment sugars [5]. There is a scarcity of papers in the literature regarding the association of R. mucilaginosa with oral ulcers. In a report from Taiwan [7] it was noted on endoscopy that oesophageal ulcers caused by R. rubra resembled ulcers caused by Candida. R. mucilaginosa, usually considered a commensal, is known to cause fungal peritonitis, endocarditis [6], fungemia [6,8–10] and meningitis [6,10] in patients undergoing chemotherapy for cancer and those with indwelling intravenous catheters [6,11], and disseminated R. mucilaginosa infection [9] and meningitis [12] in HIV patients. Eye infections caused by Rhodotorula spp. have included chronic postoperative endophthalmitis and dacryocystitis [13]. An outbreak of R. mucilaginosa in a neonatal intensive care unit was recently reported in preterm infants with indwelling catheters [14]. A positive direct microscopy and repeated isolation in pure culture pointed towards it being the causative agent. Studies have shown that Rhodotorula is susceptible to 5-fluorocytosine, is moderately susceptible to amphotericin B, miconazole, ketoconazole, and itraconazole, and is mostly resistant to fluconazole [6]. An improvement seen in the patient after a change in therapy to itraconazole emphasizes the aetiological role of the fungus in our patient. Information on the oropharyngeal and esophageal involvement of Rhodotorula in patients with HIV infection is scarce and therefore important. Although the clinical presentation is similar to infection caused by Candida, the response to treatment is different. The role of mycological evaluation and culture is thus increasingly important in cases not responding to conventional therapy, especially in reducing the morbidity in patients with AIDS with low CD4 cell counts.
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