Trichosporon asahii infection in an HIV-positive patient

Abstract

Trichosporonosis in advanced AIDS, including in a report of a patient with fatal Trichosporon asahii fungemia, was recently discussed by Gross and Kan [1]. The patients reviewed by them had a diagnosis of AIDS and, when reported, an absolute CD4 cell count of 185 cells/μl or less. We recently successfully treated catheter-related T. asahii bloodstream infection in an HIV-positive patient with a higher absolute CD4 cell count and no prior history of 0002030-defining illness. A 22-year-old man presented with an 8-month history of cough, weight loss, and recent hemoptysis. He was known to be HIV positive but had declined antiretroviral therapy. His absolute CD4 cell count (which was also his recorded nadir) was 270 cells/μl, and his HIV RNA level was 50 460 copies/ml. There were no other comorbid illnesses. He was diagnosed with pulmonary tuberculosis (TB) with a tuberculous empyema. Isoniazid, pyrazinamide, ethambutol, and rifampin were begun, and thoracostomy drainage was performed. His course was complicated by respiratory failure with development of ventilator-associated pneumonia requiring treatment with intravenous vancomycin and imipenem/cilastatin, renal failure requiring renal replacement therapy, and unremitting fevers. Culture of his hemodialysis catheter grew 75 colonies of T. asahii (Vitek2, bioMérieux, Durham, North Carolina, USA). He rapidly defervesced after the institution of amphotericin B lipid complex (5 mg/kg intravenous daily). He had marked clinical improvement with successful extubation and recovery of normal renal function. Neutropenia did not develop during the course of his illness and, following the completion of a 2-week course of amphotericin B, he was begun on antiretroviral therapy. Currently, he is doing well and completing his anti-TB regimen. Trichosporon is a basidiomycetous yeast that may be found in the environment or colonizing human skin, stool, or urine [2]. In immunocompetent individuals, Trichosporon species can produce a superficial hair shaft infection (white piedra) or summer-type hypersensitivity [3,4]. Trichosporonosis has been reported most often in patients with hematologic malignancies, especially acute myelogenous leukemia [5], and profound neutropenia, cytotoxic chemotherapy, and prolonged corticosteroid use have been identified as risk factors for disseminated disease [5,6]. The disease has also been reported in bone marrow and solid-organ transplant recipients [7,8] and in patients with severe burn injuries [9]. As discussed by Gross and Kan [1], recent changes in Trichosporon taxonomy make comparisons between current and historic cases difficult, as clinically relevant species were formerly referred to collectively as Trichosporon beigelii or Trichosporon cutaneum[8]. Although there is an increased rate of carriage of T. beigelii in homosexual men, invasive trichosporonosis in AIDS has remained rare [10]. Similar to our case, Gross and Kan [1] noted that the presence of a venous (or peritoneal) catheter might be associated with Trichosporon infection. Trichosporon species can be normal human skin flora, with asymptomatic inguinal carriage reported in up to 12.4% of individuals [11]. In patients with hematologic malignancies and trichosporonosis, the presence of central venous catheters has ranged from 3.2% to 70% [5,6]. In patients with Trichosporon fungemia, in addition to systemic antifungal therapy, central venous catheters should likely be removed to increase the likelihood of successful treatment. The presence of 0002030-defining illness seems to be a possible predisposing factor for trichosporonosis. Similar to a previous report [12], our patient had pulmonary TB. Unlike the patients reported and reviewed by Gross and Kan [1], our patient had a higher absolute CD4 cell count and never developed neutropenia. Our case seems to support the premise of Gross and Kan [1] that trichosporonosis in AIDS patients is more likely to be associated with the severity of underlying illness than with impaired cell-mediated immunity or HIV itself and with the presence of a central venous catheter than with neutropenia. The optimal treatment for Trichosporon infections is not well defined. Amphotericin B can be used, but higher minimal inhibitory concentrations have been reported in vitro. Voriconazole, and possibly posaconazole, may be superior to amphotericin B [8].