Breakthrough trichosporonosis in patients with hematologic malignancies receiving micafungin.
BACKGROUND
Micafungin is a newly approved antifungal agent in the echinocandin class that is active against Candida species and Aspergillus species. However, this agent has limited activity against a number of fungi, including Trichosporon species. We describe 4 patients who developed disseminated trichosporonosis during the use of micafungin. No cases of trichosporonosis had been seen in the 2 years prior to January 2003, when micafungin became available in our hospital.


METHODS
We reviewed microbiological records of patients at Kameda General Hospital (Kamogawa City, Chiba, Japan) from 1 January 2002 to 31 July 2005, and identified 4 patients whose blood culture results were positive for Trichosporon species.


RESULTS
Since January 2003, four patients--3 with acute myelocytic leukemia and 1 with myelodysplastic syndrome--developed disseminated trichosporonosis while receiving treatment with micafungin with or without amphotericin B. The initial 2 isolates were identified as Trichosporon beigelii, and the later 2 isolates were identified as Trichosporon asahii. All 4 patients received micafungin, and 2 also received amphotericin B concomitantly. Minimal inhibitory concentrations of micafungin were >16 microg/mL for the 2 isolates available for susceptibility testing. One patient with hematologic recovery (neutrophils >500 cells/mm3) showed elimination of the fungus after receiving treatment with voriconazole. However, the 3 other patients without hematologic or immunological recovery died of disseminated infection.


CONCLUSIONS
The rarity of trichosporonosis in our hospital and its emergence after the introduction of micafungin therapy support the idea that micafungin may exert a significant, selective pressure toward resistant fungi, such as Trichosporon species. Therefore, care should be taken regarding the possibility of trichosporonosis in patients receiving micafungin with or without amphotericin B.
Matsue
Kosei
K
Department of Hematology and Oncology, Kameda General Hospital, Kamogawa-Shi, Chiba, Japan. koseim@dc4.so-net.ne.jp
Uryu
Hidetaka
H
Koseki
Mihoko
M
Asada
Noboru
N
Takeuchi
Masami
M
D000666:Amphotericin B / Q000627:therapeutic use; D000935:Antifungal Agents / Q000627:therapeutic use*; D025141:Drug Resistance, Fungal; D004359:Drug Therapy, Combination; D054714:Echinocandins; D019337:Hematologic Neoplasms / Q000150:complications*; D006801:Humans; D007564:Japan; D055666:Lipopeptides; D008074:Lipoproteins / Q000627:therapeutic use*; D008297:Male; D000077551:Micafungin; D008826:Microbial Sensitivity Tests; D008875:Middle Aged; D009181:Mycoses / Q000150:complications / Q000188:drug therapy* / Q000382:microbiology; D010456:Peptides, Cyclic / Q000627:therapeutic use*; D012641:Selection, Genetic; D014250:Trichosporon / Q000302:isolation & purification*
D000935:Antifungal Agents; D054714:Echinocandins; D055666:Lipopeptides; D008074:Lipoproteins; D010456:Peptides, Cyclic; D000666:Amphotericin B; D000077551:Micafungin