Trichosporon Infections Clinical Presentation

Updated: Jan 16, 2015
  • Author: Ryan C Maves, MD, FACP, FCCP, FIDSA; Chief Editor: Mark R Wallace, MD, FACP, FIDSA  more...
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Presentation

History

The typical patient with trichosporonosis 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 in patients with invasive candidiasis, empiric broad-spectrum antibacterial therapy without clinical improvement may be included in the history. Prophylactic antifungal therapy with echinocandins may precede a breakthrough Trichosporon infection. [27]

White piedra is not a significant risk factor. [1]

Past medical history may include hemochromatosis [13] or prosthetic heart valve placement. [16]

Patients with trichosporonosis may have a variable constellation of historical features, depending on the organs involved, and often have fever and chills.

Pulmonary infiltrates and respiratory symptoms may be present.

Flank pain, azotemia, hematuria, or red blood cell casts may signal renal involvement. [13]

Skin involvement often begins as a discrete maculopapular rash and may progress to purpuric or hemorrhagic manifestations. [13] (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 symptomatic.

Patients undergoing peritoneal dialysis may present with abdominal pain, abdominal distension, and cloudy peritoneal fluid. [8, 28]

Chorioretinitis [13] and spondylodiscitis have also been described. [29]

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Physical

Cutaneous findings occur in one third of patients with disseminated Trichosporon disease. [30] The most commonly described lesions are nontender erythematous nodules of varying number, [26] which are located mainly on the extremities but are also found on the trunk and face. The lesions may become ulcerated, [30] with 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 but with no specific pattern of involvement. [1] Hypoxemia has been described in association with these lesions. An isolated pulmonary infiltrate may be the only demonstrable manifestation of trichosporonosis in some patients.

Flank tenderness or hematuria may be present and suggests 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.

Some patients have infection localized to only one organ, and fungemia may not occur in all of these patients. [1] Localized disease has been described in the lungs, peritoneum, [8] eye, brain, and stomach.

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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, include the following:

  • T asahii
  • B capitatus ( Trichosporon capitum)
  • T inkin
  • Trichosporon dermatis
  • Trichosporon montevideense

Trichosporon is a normal colonizer of mucous membranes in the GI and respiratory epithelium, as well as the 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’s flora. Trichosporon is not often isolated from hospital environments, although outbreaks due to contaminated hospital equipment have been reported. Unlikely sources of nosocomial spread, such as infected urinary catheters and aerosolization of the fungus, have been described. [25, 31]

Risk factors include the following:

  • Neutropenia is the greatest single risk factor. [7]
  • Additional risk factors include corticosteroid use, cytotoxic chemotherapy, diabetes, [32] and hemochromatosis. [13]
  • Trichosporonosis has been described in patients with prosthetic heart valves, [33] those with HIV infection, patients on dialysis, and neonates.
  • Many of these risk factors directly contribute to deficiencies in the host immune system. Hemochromatosis may be a risk factor owing to excess iron stores, as in vitro data suggest improved fungal growth in iron-supplemented media. [13]
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