eMedicine Specialties > Infectious Diseases > Fungal Infections

Trichosporon Infections

Author: Ryan C Maves, MD, Staff Physician and Director, Tropical Medicine Training Program, US Naval Medical Research Center Detachment, Peru
Coauthor(s): Braden R Hale, MD, MPH, Consulting Staff, Department of Internal Medicine, Division of Infectious Diseases, Naval Medical Center at San Diego
Contributor Information and Disclosures

Updated: Sep 29, 2006

Introduction

Background

Trichosporon species are soil inhabitants and common colonizers of human skin and GI tracts. Previously, all pathogenic members of the genus Trichosporon were regarded as a single species, Trichosporon beigelii. More recently, biochemical and morphologic differences within the genus have been appreciated. T beigelii has now been divided into distinct species, at least 8 of which have the potential to cause human disease: Trichosporon asahii, Trichosporon inkin, Trichosporon asteroides, Trichosporon cutaneum, Trichosporon mucoides, Trichosporon ovoides, Trichosporon pullulans, and, more recently, Trichosporon loubieri.

T asahii and T inkin have been most closely implicated with human infections. White piedra, a distal infection of the hair shaft, appears to be due to T inkin, as are other superficial infections such as dermatomycosis, onychomycosis, and otomycosis. Multiple species, including T asahii and T mucoides, are associated with summer-type hypersensitivity pneumonitis, which is commonly found in Japan.

First described in the 1960s as a cause of pulmonary mycosis, Trichosporon causes severe disseminated disease in immunocompromised individuals. T asahii is responsible for most of the invasive infections known collectively as trichosporonosis. Invasive disease caused by Blastoschizomyces capitatus, (formerly Trichosporon capitatus and also known as Geotrichum capitatum) is included in this definition. Hematologic malignancies are the strongest identified risk factor for trichosporonosis, but corticosteroid use, hemochromatosis, deficiencies of granulocyte function, and end-stage renal disease have all been implicated in its development.

Pathophysiology

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. Among the patients in a large Veterans Administration hospital, 0.8% of throat cultures and 3.1% of stool culture findings were positive for T beigelii, and other studies report similar rates.

Despite this, infection with Trichosporon is rare, even in patients with impaired host defenses. In one retrospective study, trichosporonosis (including trichosporonosis caused by B capitatus) developed in only 0.9% of patients with acute leukemia. Hematologic malignancies were associated with 62.8% of reported cases of trichosporonosis. Of the remaining cases, corticosteroid use, solid tumors, HIV/AIDS, and intravascular devices, including catheters and prosthetic heart valves, represented major risk factors. Hemochromatosis is a separate risk factor for trichosporonosis; increased concentrations of iron appear to favor the growth of Trichosporon.

Risk factors can work in conjunction; for example, cytotoxic-induced chemotherapy 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 associated with end-stage renal disease. Invasion of mucosal barriers appears to be followed by vascular invasion and local spread, which are then followed by dissemination to other sites. The liver, spleen, kidney, lungs, eye, brain, GI tract, and skin are frequently involved in the acute disseminated syndrome. In chronic forms, patients who are recovering from neutropenia cannot rid themselves of the organism and develop scattered visceral lesions similar to those observed in hepatosplenic candidiasis. Occasionally, infection may be limited to a single organ system (eg, lungs).

Frequency

United States

This disease is rare. Approximately 400 cases of invasive Trichosporon (including B capitatus) infection had been reported in the world literature, although a true estimate of disease incidence cannot be calculated. In the highest risk group (patients with hematologic malignancy), fewer than 0.1% of patients appear to contract the illness.

International

Despite the small number of cases, B capitatus may have a geographic predilection for Europe, with 86.9% of reported cases arising there (especially in Spain and Italy).

Mortality/Morbidity

• Two common variants of Trichosporon infection occur in humans: (1) a disseminated acute-onset form associated with high mortality and (2) a more indolent form that causes visceral lesions and is associated with lower mortality. Acute trichosporonosis generally disseminates to multiple organs and is fatal in more than 60% of patients. In more indolent forms, mortality rates are significantly lower but may require prolonged administration of antifungal agents.

Sex

• Invasive disease due to Trichosporon species occurs significantly more often in males, with a 2:1 male-to-female predominance being reported in multiple series. In one series, 47 of 67 (70%) cases occurred in males, with 138 of 205 (67%) cases occurring in males in a separate series. The prevalence of white piedra is also greater in male patients.

Age

• Diseases that confer susceptibility to Trichosporon infections are most prevalent in adults, and most of the reported cases occur in adults.
• A scattered number of neonatal invasive Trichosporon infections have been reported.

Clinical

History

• The typical patient presents with neutropenia and fever, usually in the setting of cytotoxic chemotherapy for a hematologic malignancy. The patient may also have an indwelling intravascular or peritoneal catheter.
• A history of corticosteroid use is common, often as part of a chemotherapeutic regimen for leukemia or lymphoma. As with patients who have invasive candidiasis, broad-spectrum antibiotic use without improvement may be included in the history. However, prophylactic antifungal therapy, such as amphotericin B or echinocandins, may have also been administered without benefit.
• White piedra is not a significant risk factor.
• Elicit information about the presence of hemochromatosis or prosthetic heart valves from patients with invasive Trichosporon infection.
• Patients may have a variable constellation of historical features, depending on the organs involved.
• Patients able to relate a history generally note the presence of fever and, possibly, chills.
• In patients with pulmonary infiltrates, symptoms of respiratory insufficiency may be present.
• Flank pain and a history of hematuria may signal renal involvement.
• A significant number of patients note skin involvement. (The presence of skin lesions may represent a site for biopsy, aiding in the diagnosis.)
• GI lesions from the oropharynx to the rectum may be a source of complaint.
• Patients undergoing peritoneal dialysis may present with abdominal pain, abdominal distension, and cloudy peritoneal fluid.

Physical

• Cutaneous findings
  • These occur in a third of patients with disseminated disease.
  • A variety of cutaneous lesions are described. The most common lesions are nontender, erythematous nodules of varying number, which are located mainly on the extremities but are also found on the trunk and face. The lesions may become ulcerated, possibly developing an appearance similar to that of ecthyma gangrenosum.
• Ocular involvement is well-described and occurs in the uveal tissues.
• Pulmonary infiltrates are common, occurring in about 25% of patients, with no specific pattern of involvement. Hypoxia has been described in association with these lesions. An isolated pulmonary infiltrate may be the only demonstrable manifestation of Trichosporon in some patients.
• Flank tenderness or hematuria may be present and suggests possible renal involvement, which is common.
• Lesions may be found along the entire length of the GI tract, usually in the form of erosions or ulcers.
• A subset of patients have infection localized to only one organ, and fungemia may not occur in all of these patients. Localized disease has been described in the lungs, peritoneum, eye, brain, and stomach.

Causes

Most literature prior to 1995 refers to pathogenic Trichosporon species as T beigelii. Subsequent articles usually describe specific species under the newer nomenclature.

• Etiologic agents, in order of reported frequency
  • T asahii
  • B capitatus
  • T inkin
• Trichosporon is a normal colonizer of mucous membranes in the GI and respiratory epithelium and skin; invasive disease usually requires significant host compromise of both anatomic and neutrophilic defenses.
• In nearly all patients, the source of the invasive organism is the host flora. Trichosporon is not typically isolated from hospital environments, although outbreaks due to contaminated hospital equipment have been reported. Unlikely sources of nosocomial spread, such as infected urinary catheters that lead to aerosolization of the fungus and airborne transmission, have been described.
• Risk factors
  • Among host factors, neutropenia is the greatest single risk factor; however, most exposed neutropenic patients remain uninfected, and a significant number of infected patients are not neutropenic.
  • Corticosteroid use is another significant risk factor. Patients receiving steroids for a variety of reasons without other predisposing factors have been infected.
  • Hemochromatosis is another risk factor, and the Trichosporon organism's growth is enhanced by supplemental iron.
  • Prosthetic heart valves have been infected with Trichosporon.
  • Infections are reported among patients infected with HIV, patients undergoing renal replacement therapy, and neonates.

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