Fatal Trichosporon asahii septicemia in a Guatemalan farmer with acute lymphoblastic leukemia.

To the Editor: Trichosporon species are found in nature; predominantly in soil, water, and on plants. They have been cultured from many animal droppings, including cattle, sheep, and goat. (1) The six Trichosporon species associated with human infection are Trichosporon asahii, Trichosporon mucoides, Trichosporon asteroides, Trichosporon cutaneum, Trichosporon inkin, and Trichosporon ovoides. Of these, Trichosporon asahii is the predominant cause of systemic, invasive human infection. (1) Invasive trichos-poronosis occurs mainly in immuno-compromised persons. Limited antifungal options exist and mortality rates remain high.

Humans can be colonized with Trichosporon species. Colonization of mucosal surfaces, stool, urine, sputum, and hair has been documented. (2) This report describes a case of fatal T asahii septicemia in a Guatemalan farmer with acute lymphocytic leukemia. He was most likely colonized with Trichosporon from his livelihood as a farmer with extensive exposure to, and handling of, cattle, sheep, and goat feces.

A 43-year-old Guatemalan man was transferred to our hospital with a five-day history of fever. He had been recently diagnosed with acute lymphocytic leukemia, and had undergone induction chemotherapy via a peripherally inserted central catheter (PICC). Upon transfer, he had been neutropenic for 21 days. Medications included piperacillin-tazobactam and vancomycin. The patient was a cattle, sheep, and goat farmer from a village in rural Guatemala. He had emigrated to the United States 4 months prior.

Physical examination revealed a temperature of 39[degrees]C, splenomegaly, and an intact PICC. Laboratory studies revealed a white blood cell count of 100 cells/[mm.sup.3] (normal 4,500-11,000 cells/[mm.sup.3]) with 10% neutrophils, hemoglobin 8.8 g/dL (normal, 13.6-17.5 g/dL), and platelets 26,000/[mm.sup.3] (normal 150,000-450,000/[mm.sup.3]). All other routine laboratory tests and CT scans (chest, abdomen, pelvis, sinuses, and brain) were negative. All previous blood, sputum, and urine cultures were negative.

The patient remained febrile. On day 6, he became progressively dyspneic and tachypneic. Multiple red papular lesions appeared diffusely. Repeat CT scans revealed two new peripheral right lung nodules. Liposomal amphotericin-B was added, but hypotension and respiratory failure ensued. On days 8 and 9, multiple blood cultures (peripheral and PICC) grew urease-positive yeast. The PICC was removed and the tip sent for culture. Urine culture also grew urease-positive yeast. Biopsies of the skin lesions and bone marrow (Fig. 1) were performed.

T asahii was isolated from the blood, urine, and PICC tip cultures, as well as from the skin and bone marrow biopsies. Voriconazole was substituted for liposomal amphotericin-B. Unfortunately, the patient died due to multiorgan failure from T asahii septicemia.

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Invasive trichosporonosis occurs mainly in immunocompromised persons. Neutropenic patients with hematologic malignancies account for 90% of cases. (1-6) Other risk factors include HIV infection, organ transplantation, burns, IV eatheters, chronic ambulatory peritoneal dialysis, corticosteroid treatment, and heart valve surgery. (7-13)

Invasive trichosporonosis is typically heralded by an acute febrile illness that is unresponsive to empiric antibacterial agents. Skin lesions occur in one-third of patients. Multiorgan failure (usually pulmonary and renal) and sepsis develop rapidly. Mortality rates can approach 100% depending on the patient's underlying condition (especially if it involves prolonged neutropenia), time to diagnosis, and burden of disease. (3-6)

Trichosporon species grow readily on standard fungal media. Trichosporon, Cryptococcus, Histoplasma, and Malassezia species are all urease-positive yeast. Trichosporon species form arthroconidia, blastoconidia, hyphae, and pseudohyphae. Cryptococcus, Histoplasma, and Malassezia do not. Therefore, a urease-positive yeast that forms arthroconidia can be presumptively identified as a Trichosporon species. (1-5)

Invasive trichosporonosis is difficult to treat. T asahii, the predominant cause of invasive trichosporonosis, is resistant to amphotericin. (1-6,14,15) Echinocandins are inactive against Trichosporon species. (15,16) Azole drugs have in vitro activity and in vivo efficacy against Trichosporon species. (16-22) High-dose azole therapy (fluconazole 600-1000 mg/d; voriconazole 4-6 mg/kg every 12 hours) is recommended for patients with invasive trichosporonosis; (21,22) however, the overall prognosis remains poor. The few patients who have survived were either not neutropenic at the time of diagnosis or recovered from their neutropenia shortly after the infection was diagnosed.

Acknowledgment: I wish to acknowledge Dr. Philip A. Mackowiak for his review of the manuscript.

Kirk M. Chan-Tack, MD

Institute of Human Virology 

University of Maryland School of Medicine

Baltimore, MD

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