Background
Trichosporon species are fungi that commonly inhabit the soil. They colonize the skin and gastrointestinal tract of humans. [1, 2] Long known as the cause of superficial infections such as white piedra, a distal infection of the hair shaft, [3] the genus is now the second most commonly reported cause of disseminated yeast infections in humans. [4]
Trichosporon species are widely distributed in nature. Commonly isolated from soil and other environmental sources, Trichosporon is also a commensal in the human gastrointestinal and respiratory tracts. [1] Among the patients in a large Veterans Administration hospital, 0.8% of throat cultures and 3.1% of stool culture findings were positive for Trichosporon beigelii. [5] A study of patients with cancer found a similar colonization rate of 3.7%. [6]
All pathogenic members of the genus Trichosporon were once regarded as a single species, T beigelii. [7] Biochemical and morphologic differences within the genus have led to the division of the former T beigelii into distinct species, at least 9 of which have the potential to cause human disease: Trichosporon asahii (the most common cause of disseminated disease), Trichosporon inkin (the cause of white piedra [8] ), Trichosporon asteroides, Trichosporon cutaneum, Trichosporon mucoides, Trichosporon ovoides, Trichosporon pullulans,Trichosporon loubieri, and Trichosporon japonicum. [9]
Multiple Trichosporon species, including T asahii and T mucoides, are associated with summer-type hypersensitivity pneumonitis in Japan. [10] Blastoschizomyces capitatus (formerly known as Trichosporon capitatus and also known as Geotrichum capitatum) is a closely related pathogen, and invasive B capitatus disease shares risk factors and clinical features with trichosporonosis. [11]
First described in the literature as a cause of invasive disease in 1970, [12] Trichosporon species are increasingly recognized as a cause of systemic illness in immunocompromised patients. [7] Hematologic malignancies are the best-described risk factors for trichosporonosis, [7] accounting for 63% of reported cases. Additional risk factors include corticosteroid use, hemochromatosis, other deficiencies of granulocyte function, HIV/AIDS, and end-stage renal disease. [13, 14]
Pathophysiology
Trichosporon species have various putative virulence factors. Enzyme products of Trichosporon include proteinases, lipases, and phospholipases, but the specific contribution of an individual enzyme to human disease remains unclear. The cell wall of Trichosporon contains a 1,3-linked mannose backbone similar to that of Cryptococcus neoformans that inhibits phagocytosis by macrophages in a murine model. Biofilm production by Trichosporon facilitates colonization of indwelling devices, permitting both adherence to prosthetic material and reduction of the fungus’s exposure and susceptibility to antifungal drugs. [15]
In most cases of severe disease, multiple risk factors favor the development of tissue invasion; for example, chemotherapy used to treat hematologic malignancies can cause neutropenia and mucosal disruption. Trichosporon peritonitis is described in association with peritoneal dialysis catheters and is likely related to the combination of disrupted barrier immunity and immune dysfunction due to end-stage renal disease. [8] This invasion of mucosal barriers appears to be followed by vascular invasion and dissemination to other sites. Occasionally, Trichosporon infections are limited to a single organ system (eg, the lungs), but scattered visceral lesions similar to those observed in hepatosplenic candidiasis can also occur, often in patients who are recovering from neutropenia and cannot clear the infection.
Epidemiology
Frequency
Trichosporon infections are rare, even among patients with impaired host defenses. Corticosteroid use, solid tumors, HIV/AIDS, and intravascular devices, including catheters and prosthetic heart valves, [16] are other major risk factors. In one retrospective series, trichosporonosis (including B capitatus infections) developed in only 0.9% of patients with acute leukemia. [17] In another review of yeast bloodstream infection in patients with cancer at a major referral center, Trichosporon was identified in only 8 of 2,984 isolates (0.27%). Hematologic malignancy is the best-described risk factor. [18]
Despite the small number of cases, B capitatus may have a geographic predilection for Europe, with most reported cases arising there (especially in Spain and Italy).
T asahii may be a more common cause of breakthrough fungemia in neutropenic patients from Japan than other regions, [19] and this organism is the cause of summer-type hypersensitivity pneumonitis, a condition reported exclusively in Japan. [10]
Mortality/Morbidity
The mortality rate of acute disseminated trichosporonosis has been previously documented at between 50% and 80% in most case series. [20, 21, 22] More recent series have reported mortality rates of 40%-50% in patients with invasive disease. [23, 24]
Sex
Trichosporonosis is much more common in males, with a 2:1 male-to-female predominance reported in multiple series. [13, 21]
Age
Diseases that confer susceptibility to Trichosporon infections are most prevalent in adults, with a median age of 44 years in one report. [21]
A small number of neonatal and pediatric invasive Trichosporon infections have been reported, including nosocomial outbreaks within neonatal intensive care units. [25, 26]
