Trichosporon Infections

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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

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]

Epidemiology

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]

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]

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.

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:

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:

Laboratory Studies

The diagnosis of trichosporonosis is usually confirmed by a positive blood culture result obtained in the evaluation of a febrile (typically neutropenic) patient.

Important laboratory tests include blood culture sets, blood chemistries and hepatic transaminases, alkaline phosphatase, bilirubin, lactic acid dehydrogenase (LDH), and urinalysis with urine culture.

Urine cultures may be the first to grow Trichosporon in the setting of disseminated disease,[6] and it should not be presumed to be a contaminant or colonizer in the high-risk host (ie, in the setting of neutropenic fever).[1]

Trichosporon and C neoformans are closely related organisms and share a number of surface antigens. As such, the latex agglutination test results for serum cryptococcal antigen is often positive in the setting of disseminated trichosporonosis[7] (except trichosporonosis due to B capitatus[11] ). This widely used, rapid, and inexpensive test may provide an early clue about a Trichosporon infection. Because of changes in cell wall conformation, these test results may become negative during antifungal therapy, but newly negative test results do not imply a response to therapy.[1]

Investigational methods of rapid molecular diagnostics, such as DNA-based microarrays,[34] polymerase chain reaction (PCR), and pyrosequencing,[35] are in development but are not yet widely available for clinical use.[36, 37]

Imaging Studies

Radiologic evaluation should include a chest radiograph and CT scans of the abdomen and pelvis. A CT scan of the chest is also frequently useful in the evaluation of the pulmonary infiltrate in the patient population at risk for Trichosporon infection, but confirmation of the diagnosis should rely on a tissue sample or on another useful clinical sample. Depending on the clinical picture, a CT scan or MRI of the brain may be indicated.

Endocarditis is rarely reported[16, 33] but is associated with high mortality rate (82% in a single series). Patients with prosthetic heart valves or persistently positive blood culture results should undergo echocardiography.

Procedures

Bronchoscopy

When pulmonary infiltrates are present, bronchoscopy is a useful means of obtaining samples if the patient can tolerate the procedure. Positive culture results from a bronchial lavage support the diagnosis.[26]

Biopsy

Open-lung biopsy may be required for definitive diagnosis because of the large number of viral, bacterial, protozoal, and fungal pathogens that can cause disease in patients with pulmonary infiltrates.

Lesions of the GI tract may be accessible for biopsy and may yield a diagnosis before blood cultures return positive findings.

Skin lesions occur in roughly 10% of patients with disseminated trichosporonosis. Biopsy of suspicious lesions in immunocompromised patients with fever may facilitate early diagnosis.

Liver lesions or other visceral lesions may also require biopsy for diagnosis and optimal management.

Histologic Findings

Grossly, infected tissues may contain micronodules (0.5-1.0 cm), occasionally surrounded by red rims. The GI tract may demonstrate ulceration and erosion associated with hemorrhage and hemorrhagic infarction.[7]

Microscopic examination of a nodule may reveal a necrotic center with fungal elements either in a starburst pattern or more loosely organized. Fungal elements may be observed invading the vasculature. Visualization of blastoconidia, arthroconidia, hyphae, and pseudohyphae in a histologic section supports the diagnosis of invasive Trichosporon infection.[7, 13] The cellular inflammation surrounding the fungal elements may vary, occasionally associated with hemorrhage. Granulomatous inflammation with multinucleated giant cells has been reported.[38]

Medical Care

Voriconazole and posaconazole show excellent in vitro activity against Trichosporon.[16, 24, 26, 39] In particular, voriconazole seems to have better in vitro activity than amphotericin B.[24, 40, 41] Indeed, successful clearance of fungemia with voriconazole has been reported when liposomal amphotericin B treatment was failing.[26] Posaconazole is approved by the US Food and Drug Administration for prophylaxis of invasive Aspergillus and Candida infections in patients at high risk because of severe immunosuppression and has activity against Trichosporon, although human clinical data are both limited and mixed in terms of results.[42, 43]

High-dose amphotericin B deoxycholate (1-1.5 mg/kg/d) historically has been the most common treatment for invasive trichosporonosis, but many breakthrough cases have occurred on this therapy.[22, 44] Because of high rates of resistance to amphotericin B[40] and the toxicity of this regimen, alternate therapies are often necessary. Lipid preparations of amphotericin B (eg, liposomal amphotericin B, 5 mg/kg/d) are commonly used in place of amphotericin B deoxycholate, although treatment failures have also been reported with these agents.[20] Bcapitatus infections appear to respond better to amphotericin B than those due to Trichosporon species.[22]

The echinocandins caspofungin and micafungin have poor in vitro activity against Trichosporon when used alone.[19] One report describes successful treatment of T inkin peritoneal catheter–associated peritonitis using caspofungin monotherapy.[8] However, cases of breakthrough T asahii infections have been reported in patients with hematologic malignancies receiving micafungin[19] and caspofungin[32] for empiric treatment of neutropenic fever. Combination therapy with caspofungin and liposomal amphotericin B may be effective,[20] and micafungin and amphotericin B appear synergistic against Trichosporon in vitro. One in vivo murine model of trichosporonosis showed a significant reduction in fungal burden in multiple infected organ systems when amphotericin B was combined with micafungin.

Combination therapy should be the cornerstone of treatment for trichosporonosis. The combination of high-dose amphotericin B (deoxycholate or liposomal) with either or both 5-flucytosine or voriconazole is commonly prescribed, although failure rates remain high. Amphotericin B plus an echinocandin is a potentially promising regimen, and synergy has been suggested in vitro[45] and in a murine model,[46] with a small number of successful reports of salvage therapy in the current literature.[47, 48]

Regardless of the therapeutic options, patients’ clinical responses may not be optimal until they recover from their predisposing immunocompromised states. Possible strategies include the addition of granulocyte colony-stimulating factor (G-CSF) in patients with neutropenia[7] and the reduction of glucocorticoid doses as much as possible in patients receiving these agents. Persistence of positive blood culture findings on amphotericin B monotherapy suggests resistance, and modification of the regimen is indicated. Catheter-associated infections, such as peritonitis in patients undergoing peritoneal dialysis, generally require removal of the catheter.

In patients who do not respond to high-dose amphotericin B, an azole or flucytosine (5-FC) should be added. Unfortunately, all of these therapies have significant failure rates in patients with neutropenia. levels of 5-FC must be carefully monitored. Do not use 5-FC if levels cannot be measured expeditiously. Liposomal amphotericin has been successfully used in trichosporonosis but may not necessarily offer greater efficacy over standard therapy. Miconazole has significant in vitro activity; however, this does not translate to useful in vivo results, and it should not be used.

Consultations

Patients with trichosporonosis are often critically ill because of their infection and their frequent underlying illnesses. ICU admission is warranted in most cases.

Proper management should include input from an infectious disease specialist.

Consultation with an ophthalmologist is generally advised for diagnostic purposes and to evaluate for fungal retinitis.

Because of the many organ systems involved, input from a number of other specialists may be required. Pulmonologists, intensivists, gastroenterologists, dermatologists, and general surgeons commonly assist in the diagnosis and management of patients with trichosporonosis.

Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications. In general, empiric monotherapy should be avoided without specific testing of fungal sensitivity to available drugs.

Amphotericin B (Amphocin, Fungizone)

Clinical Context:  Amphoteric polyene antifungal with activity against many fungal pathogens. Administered in solution only and is well known for a variety of toxic side effects. May be injected intrathecally or into a joint space, or it may be used as an irrigant, although it is usually administered IV. Dose should be adjusted for the indication. For trichosporonosis, high doses are required. Lipid formulations of amphotericin B (see below) are generally preferred, however.

Amphotericin B, liposomal (AmBisome)

Clinical Context:  Lipid formulations of amphotericin B that deliver higher concentrations of the drug, with a theoretical increase in therapeutic potential and decreased nephrotoxicity. Produced from a strain of Streptomyces nodosus. Antifungal activity of amphotericin B results from its ability to insert itself into fungal cytoplasmic membrane at sites that contain ergosterol or other sterols. Aggregates of amphotericin B accumulate at sterol sites, resulting in an increase in cytoplasmic membrane permeability to monovalent ions (eg, potassium, sodium).

At low concentrations, the main effect is increased intracellular loss of potassium, resulting in reversible fungistatic activity; however, at higher concentrations, pores of 40-105 nm in cytoplasmic membrane are produced, leading to large losses of ions and other molecules. A second effect of amphotericin B is its ability to cause auto-oxidation of the cytoplasmic membrane and release of lethal free radicals. Main fungicidal activity of amphotericin B may reside in ability to cause auto-oxidation of cell membranes.

Voriconazole (Vfend)

Clinical Context:  A triazole antifungal agent that inhibits fungal cytochrome P450-mediated 14 alpha-lanosterol demethylation, which is essential in fungal ergosterol biosynthesis. Commonly used in the treatment of aspergillosis, invasive candidiasis, and neutropenic fever. Has excellent MICs against Trichosporon species and has occasionally been effective as monotherapy.

Posaconazole (Noxafil)

Clinical Context:  Triazole antifungal agent. Blocks ergosterol synthesis by inhibiting the enzyme lanosterol 14-alpha-demethylase and sterol precursor accumulation. This action results in cell membrane disruption. Available as oral susp (200 mg/5 mL). Indicated for prophylaxis of invasive Aspergillus and Candida infections in patients at high risk because of severe immunosuppression.

Fluconazole (Diflucan)

Clinical Context:  Triazole derivative with high enteral bioavailability used for Candida infections and infections with endemic mycoses. Also useful for Trichosporon infections. Dose depends on the indication. For trichosporonosis, the dose should be the maximum dosage.

Flucytosine (Ancobon)

Clinical Context:  Pyrimidine analog available enterally or IV for use against a variety of fungal pathogens but is not generally used as monotherapy owing to emergence of resistance during therapy. Well absorbed orally but should be administered IV to critically ill patients.

Caspofungin (Cancidas)

Clinical Context:  Routinely used to treat refractory invasive aspergillosis and invasive candidiasis. First of a new class of antifungal drugs (glucan synthesis inhibitors). Inhibits synthesis of beta-(1,3)-D-glucan, an essential component of fungal cell wall.

Micafungin (Mycamine)

Clinical Context:  Member of new class of antifungal agents, echinocandins, that inhibit cell wall synthesis. Inhibits synthesis of 1,3-beta-D-glucan, an essential fungal cell wall component not present in mammalian cells.

Approved indications include (1) prophylaxis of candidal infections in patients undergoing hematopoietic stem cell transplantation and (2) treatment of esophageal candidiasis.

Further Inpatient Care

Patients with trichosporonosis should be monitored carefully, preferably in the ICU, until recovery of an adequate neutrophil count. Continue active antifungal therapy during the period of neutropenia and after recovery of neutrophil count until the resolution of symptoms.

Monitor blood cultures, urine cultures, and cutaneous or ocular lesions, along with renal and hepatic panel blood chemistries.

CT scanning of the abdomen and pelvis is indicated in most patients for initial evaluation and should be periodically repeated to monitor the progress of disease. For example, the lesions of hepatosplenic disease may become visible only after recovery of neutrophils.

The patient should remain on therapy until clinically stable and afebrile with the resolution of all visceral lesions.

Prognosis

The prognosis of acute disseminated Trichosporon infection is poor, unless recovery of neutrophils occurs.

The prognosis of indolent or localized infection is better than that of disseminated disease.

Author

Ryan C Maves, MD, FACP, FIDSA, Attending Physician, Infectious Diseases and Critical Care Medicine, Naval Medical Center San Diego; Assistant Professor of Medicine and Preventive Medicine, Uniformed Services University of the Health Sciences

Disclosure: Nothing to disclose.

Specialty Editors

Jeffrey M Zaks, MD, Clinical Associate Professor of Medicine, Wayne State University School of Medicine; Vice President, Medical Affairs, Chief Medical Officer, Department of Internal Medicine, Providence Hospital

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Thomas M Kerkering, MD, Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Mark R Wallace, MD, FACP, FIDSA, Clinical Professor of Medicine, Florida State University College of Medicine; Clinical Professor of Medicine, University of Central Florida College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Braden R Hale, MD, MPH, Director, Department of Defense HIV/AIDS Prevention Program, Naval Health Research Center, San Diego, California.

Braden R Hale, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Armed Forces Infectious Diseases Society, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Tyler E Warkentien, MD, MPH, Attending Physician, Department of Infectious Diseases, Walter Reed National Military Medical Center, Bethesda, MD

Tyler E Warkentien is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Armed Forces Infectious Diseases Society, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

DISCLAIMER

The views expressed in this article are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, nor the U.S. Government. The author of this work is an employee of the U.S. Government. This work was prepared as part of his official duties. Title 17 U.S.C. § 105 provides that ‘Copyright protection under this title is not available for any work of the United States Government’. Title 17 U.S.C. § 101 defines a U.S. Government work as a work prepared by a military service member or employee of the U.S. Government as part of that person’s official duties.

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