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Journal of Clinical Microbiology, February 2003, p. 857-859, Vol. 41, No. 2
0095-1137/03/$08.00+0 DOI: 10.1128/JCM.41.2.857-859.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Departments of Laboratory Medicine,1 Internal Medicine, National Taiwan University Hospital,2 School of Medical Technology, National Taiwan University College of Medicine, Taipei, Taiwan3
Received 8 July 2002/ Returned for modification 3 October 2002/ Accepted 21 October 2002
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Case report. A 51-year-old man was found to have nasopharyngeal carcinoma in May 1990 and received radiotherapy and intensive chemotherapy from June to August 1990. He was healthy for the following 7 years. Unfortunately, multiple bone metastases were noticed in January 1998. He received local radiotherapy for bone lesions and eight courses of chemotherapy with various regimens from July 1998 to July 1999. A Port-A-Cath catheter (Smiths Industries Medical Systems [SIMS] Deltec, Inc., St. Paul, Minn.) was implanted in June 1999. From June 1999 to October 2000, he was admitted to the hospital three times due to facial cellulitis (caused by group G Streptococcus on one occasion and of unknown etiology on two occasions) and was treated successfully with antibiotics. The catheter was flushed each time during his monthly visits to the oncology clinic.
On 18 November 2000, 1 day after the catheter was flushed, he developed a fever and visited the emergency department. There were no obvious inflammatory signs over the catheter site. His white blood count was 4,200/mm3 with 78% neutrophils. The fever disappeared spontaneously within 1 day. Culture of one blood specimen aspirated via the catheter during the febrile period was inoculated into one BACTEC Myco/F Lytic bottle (Becton Dickinson, Sparks, Md.), which yielded a red yeast (Rhodotorula species) (isolate A). Fever recurred 5 days later and again disappeared spontaneously. Blood cultures collected from peripheral veins and from the catheter at the emergency department also yielded red yeasts 5 days after incubation (the isolates were not preserved). He returned to the outpatient clinic on 29 November 2000 and remained afebrile. Fluconazole (200 mg per day) was administered orally beginning on 30 November. Unfortunately, fever up to 38.3°C occurred on 3 December and he was admitted to the hospital.
After admission, Port-A-Cath-related fungemia was suspected. Removal of the vascular catheter and treatment with amphotericin B were recommended, but the patient insisted on keeping the catheter and remaining on fluconazole therapy because of fear of the informed side effects of amphotericin B. Intravenous fluconazole (400 mg per day) was given immediately after blood cultures were performed. His fever subsided 2 days later. Five days after the patient's fever had subsided, cultures from the blood also yielded a red yeast, which was identified as R. glutinis (isolate B) (see below). Two blood cultures performed on the 7th and 12th days after initiation of intravenous fluconazole did not disclose the presence of the red yeast. The catheter was subsequently removed on the 17th day of hospitalization, and cultures of blood drawn from peripheral veins and the catheter and of blood-like material between the disk and metal portions of the catheter were also done. A Gram stain of the blood-like material disclosed many yeast-like organisms, which were later found to be red yeasts (isolate C). The culture of blood drawn from the catheter and peripheral veins did not yield the organism. The patient remained afebrile after initiation of fluconazole therapy, and the drug treatment was continued for about 4 weeks. He was discharged on 29 December 2000, and oral fluconazole (600 mg per day) was administrated for an additional 4 weeks. Two sets of blood cultures were collected 1 month after discontinuation of fluconazole therapy and were negative for the organism. At the 3-month follow-up, there was no evidence of recurrence.
Microbiology. All isolates (A, B, and C) were identified as R. glutinis by use of conventional methods (orange colonies on Sabouraud dextrose agar at 25°C and oval budding cells without pseudohyphae on cornmeal-Tween 80 agar [Difco Laboratories, Detroit, Mich.]) and API ID32 C (code number 5475750313; probability of species identification, 99.7%; typicality index, 99.6%) (bioMerieux, Marcy I'Etoile, France). For comparison, two isolates of R. glutinis (one blood isolate [D] and one isolate from pus [E] recovered from two patients seen at the National Taiwan University Hospital in 1999 and 2000, respectively) were also included in the study as control strains. The MICs for these isolates, determined by the E test (PDM Epsilometer; AB Biodisk, Solna, Sweden), were measured on RPMI 1640-2% glucose agar medium supplemented with morpholinepropanesulfonic acid (MOPS) as previously described (6). The MICs were read after 2 days of incubation at 37°C. Measurement of the MICs of fluconazole for these isolates was also performed using the methods recommended by the National Committee for Clinical Laboratory Standards (11). Random amplified polymorphic DNA (RAPD) patterns of these isolates were determined by arbitrarily primed PCR as described previously (6). The three oligonucleotide primers used, M13 (5'-GAGGGTGGCGGTTCT-3'), OPH-15 (5'-AATGGCGCAG-3'), and OPH-19 (5'-CTGACCAGCC-3') were chosen from 20 primers in a kit (OPH-1 to OPH-20) purchased from Operon Technologies, Inc. (Alameda, Calif.).
Isolates A, B, and C had identical antibiotypes: amphotericin B MICs of 0.125 µg/ml, fluconazole MICs of >256 µg/ml (the MICs determined by the E test and the NCCLS method were identical), ketoconazole MICs of 0.25 µg/ml, itraconazole MICs of 8 µg/ml, and flucytosine MICs of 0.06 µg/ml. However, for isolates D and E, the itraconazole MICs were 0.5 and 1 µg/ml, respectively, while the MICs of the other four agents were within one to two twofold dilutions of those for isolates A, B, and C. Isolates A, B, and C had identical RAPD patterns (they shared every band), and these patterns were different from those of the three control isolates (Fig. 1).
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Previous susceptibility studies of Rhodotorula species have shown that all tested isolates were susceptible to amphotericin B (MICs ranged from 0.125 to 1.6 µg/ml), ketoconazole (MICs of 
0.25 µg/ml), itraconazole (MICs ranged from 0.25 to 12.8 µg/ml), and flucytosine (MICs of 0.25 µg/ml) and resistant to fluconazole (MICs of 
32 µg/ml) (4). Among the 13 R. glutinis isolates tested by Galan-Sanchez et al. (4), 92.3% were highly resistant to fluconazole (MICs of 256 µg/ml). The susceptibility results for our isolates, i.e., high-level resistance to fluconazole and high MICs of itraconazole, were consistent with these previous findings (4). Fluconazole is not recommended as the drug of choice for the treatment of infections due to Rhodotorula species (2, 4, 9, 13). In one previous report, fluconazole failed to clear R. glutinis within a central venous catheter, which led to recurrent sepsis 5 days after the initiation of fluconazole treatment, necessitating subsequent amphotericin B treatment in a nonneutropenic patient with acute leukemia (13). The initial satisfactory improvement of our patient's clinical condition was the reason why we continued fluconazole therapy for him.
Although strains of Rhodotorula species have been shown to cause a variety of severe infections in humans, these organisms have frequently been reported as contaminants in culture plates or medical equipment because of their ubiquitous existence in the natural environment and have been known to cause nosocomial pseudoepidemics (1, 2, 4, 7, 14; Cowan and Allen, letter). In our patient, R. glutinis might have entered into the bloodstream via repeated flushing with contaminated normal saline or via an inadequately disinfected skin surface and then further multiplied and persisted within the catheter.
In conclusion, we report a microbiologically documented central venous catheter-related infection caused by R. glutinis in a nonneutropenic cancer patient. Although the isolate was highly resistant to fluconazole in vitro, this agent (high dose) was able to clear the organism from the bloodstream and the patient received fluconazole treatment for 8 weeks and had the catheter removed. Amphotericin B remains the most active agent against this organism and should be used as the treatment of choice.
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