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Infections due to Trichosporon species and Blastoschizomyces capitatus (Saprochaete capitata)

Infections due to Trichosporon species and Blastoschizomyces capitatus (Saprochaete capitata)
Literature review current through: Jan 2024.
This topic last updated: Sep 08, 2022.

INTRODUCTION — Trichosporon species and Blastoschizomyces capitatus are related fungi and are rare causes of invasive infection in humans. Both can be a constituent of the normal microbiota but can also cause both superficial and invasive infections in humans. Invasive disease due to Trichosporon spp, called trichosporonosis, occurs almost exclusively in immunocompromised hosts, appears to be increasing in frequency, and is usually fatal. This fungus also causes a characteristic infection of hair shafts called white piedra.

The mycology, epidemiology, and clinical infections caused by both Trichosporon spp and the related fungus B. capitatus will be reviewed here.

There are two other distinct but related organisms that are very rare causes of invasive human infection called Saprochaete clavata and Geotrichum candidum. Because of the rarity of infection due to these two organisms and the significant overlap in treatment, we will not mention them further. Information on diagnosis and treatment of these organisms can be found in the international guidelines on the diagnosis and management of rare yeast infections [1].  

NOMENCLATURE — The nomenclature for the organism originally called B. capitatus has evolved over the past few years, and newer reports refer to it as Saprochaete capitata or Magnusiomyces capitatus. It has been also called Geotrichum capitatum and Saprochaete capitata, and the teleomorph has been referred to as Dipodascus capitatus and Magnusiomyces capitatus. Although confusing, all of these five names (B. capitatus, Geotrichum capitatum, Saprochaete capitata, Dipodascus capitatus, and Magnusiomyces capitatus) refer to the same organism. 

At present, the correct taxonomic name is S. capitata, and that is the name more commonly referenced in the recent literature. However, in this topic we will continue to use the older name, Blastoschizomyces, because that remains the most commonly used term referenced in the literature.

MYCOLOGY — The mycology of Trichosporon spp is extremely complicated because the designation refers to a heterogeneous group of organisms. The heterogeneity results from the absence of simple methods to distinguish among the species in the clinical microbiology laboratory; thus, multiple members of the genus Trichosporon were previously categorized together under the name Trichosporon beigelii. With the use of modern molecular techniques, some mycologists have proposed a rearrangement of the genus [2-4]. The proposed names for the six main species associated with human infection are Trichosporon asahii, Trichosporon asteroides, Trichosporon cutaneum, Trichosporon inkin, Trichosporon mucoides, and Trichosporon ovoides [2,3]. The following disease associations have been observed:

T. asahii and T. mucoides are associated with systemic infection; T. asahii is more common than T. mucoides.

T. inkin and T. ovoides are associated with white piedra, affecting hair shafts; T. ovoides with infection of the hair of the scalp; and T. inkin with infection of the pubic hair.

T. asteroides and T. cutaneum are associated with superficial skin lesions.

T. ovoides has been implicated in a few cases of systemic infection [5,6].

A novel member of the genus, Trichosporon mycotoxinivorans, has been described as a pulmonary pathogen with an apparent predilection for patients with cystic fibrosis [7].

Members of the genus Trichosporon are characterized by the formation of arthroconidia, blastoconidia, hyphae, and pseudohyphae. The genus Trichosporon is closely related to Cryptococcus [8,9]. These two fungi share some antigens, and cross-reactivity with the cryptococcal polysaccharide latex agglutination assay can be seen in patients with trichosporonosis [10]. Trichosporon do not ferment carbohydrates but can assimilate various complex sugars. There is no sexual state known for the genus.

Isolation of this fungus from clinical specimens is relatively easy since it grows rapidly on almost all standard fungal media. Colonies usually appear as ivory to beige and moist with radiating furrows over time. Microscopic examination of all isolates shows nonbranching, septate, hyaline hyphae that disarticulate to form arthroconidia. Pseudohyphae and blastoconidia can also be seen.

In clinical specimens, a yeast-like organism that is urease positive and forms arthroconidia can be presumptively identified as Trichosporon spp. The identification can then be confirmed with tests of carbohydrate assimilation using commercially available kits. Distinguishing among the proposed species is not currently performed in most clinical laboratories, but guidelines for doing so have been published [3].

With widespread use and more robust databases for matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, the identification of these fungi to the species level is now possible for the laboratory and more readily available to clinicians [11].

B. capitatus can easily be mistaken for Trichosporon spp because the microscopic appearance is similar. Similar to the Trichosporon species, B. capitatus grows quickly on most mycologic media. Colonies are white, can be smooth or wrinkled, and aerial mycelia can be visible after several days of growth. Microscopically, there are septate, branching hyphae that disarticulate to form arthroconidia. If specialized conidial structures called annelloconidia are seen, this suggests B. capitatus [12] and distinguishes B. capitatus from Trichosporon spp [12]. Another important distinguishing factor is the urease test; all Trichosporon species are urease positive, and B. capitatus is always urease negative. B. capitatus is classified as an ascomycete based upon the production of asci by the teleomorph [13].

EPIDEMIOLOGY — Trichosporon spp can be found as a constituent of normal flora but can also cause both superficial and invasive infections in humans.

Source of infection − Both Trichosporon spp and B. capitatus are found in nature, predominantly in soil. There does not appear to be any association with animals, although these fungi have been cultured from animal droppings. Often, endogenous microbiota are the likely source of infection, as many patients have been shown to carry Trichosporon spp prior to the diagnosis of trichosporonosis. However, pseudo-outbreaks due to Trichosporon spp have occurred as a result of improperly sterilized endoscopes [14,15]. There have also been hospital outbreaks of trichosporonosis in immunocompromised hosts, and therefore careful adherence to infection control practices is paramount to protect patients at risk for invasive disease caused by Trichosporon spp [16].

Colonization − Humans can be colonized with Trichosporon spp and B. capitatus. Mucosal surfaces, stool, sputum, and hair have all been reported as sites of colonization. Rates of colonization vary from 1 to 3 percent in patients admitted to general hospital wards [17,18]. However, higher rates have been reported in other patient populations. A study of inguinal skin scrapings from asymptomatic outpatient volunteers in Houston showed Trichosporon colonization rates of 12.4 percent [19]. Another study, done in a Danish sexually transmitted diseases clinic, found rectal colonization rates with Trichosporon spp of 13 percent in gay males and 2.5 percent in straight males [20].

Superficial infections − Superficial infections due to Trichosporon spp occur primarily in immunocompetent patients in tropical climates. Some temperate areas, especially the southeastern United States, also have a relatively high prevalence of these superficial infections. White piedra, especially involving the genital area, appears to be most commonly found in young men [19,21]. These superficial infections appear to be sporadic and probably result from asymptomatic carriage of the organism in the hair and skin. Person-to-person spread of superficial Trichosporon spp infections does not occur.

Invasive infections − Invasive trichosporonosis occurs almost exclusively in immunocompromised patients. The majority of cases have been seen in patients with hematologic malignancies, often in the setting of neutropenia [6,22-24]. Other reported risk factors include:

AIDS [25,26]

Extensive burns [27]

Intravenous catheters [24,28-30]

Glucocorticoid treatment [23]

Heart valve surgery [31,32]

B. capitatus does not cause localized infection as noted with Trichosporon spp but does cause systemic illness, and almost all of the affected patients have had some underlying immunocompromising condition, usually neutropenia. The number of reported cases is quite small, most occurring in Italy [22]. Cardiac valve replacement in immunocompromised patients has also led to disseminated infection with this fungus [12]. There have been rare descriptions of infection due to Blastoschizomyces in apparently immunocompetent patients [33,34]. However, this fungus can be a contaminant and/or colonizer in nonsterile clinical specimens, such as sputum; thus, there must be a degree of suspicion about the diagnosis in immunocompetent patients unless there is some demonstration of tissue invasion.

Hypersensitivity pneumonitisTrichosporon spp have been implicated as a cause of hypersensitivity pneumonitis in Japan [35]. It appears that individuals, perhaps with an underlying genetic predisposition, can react to Trichosporon antigens with a resulting pneumonitis. When rigorous efforts were made to eliminate the organism from the homes of affected patients, the incidence of the disease decreased. It is unclear whether this entity exists outside of Japan.

PATHOPHYSIOLOGY — In white piedra, Trichosporon spp begins to grow just beneath the cuticle of hairs shafts. Growth continues outside the hair shaft and a nodule is formed. These nodules can easily be pulled off the hair but, when left in place, the hair shaft becomes weakened and breaks at the site of the nodule [21]. There are suggestions that strains of Corynebacterium can enhance the growth of Trichosporon spp and may play a synergistic role in white piedra [36].

Most invasive Trichosporon spp infections probably start with colonization of mucosal or cutaneous surfaces, with a break in the integrity of the surface subsequently seeding the bloodstream. Such breaks may be secondary to chemotherapy-induced mucosal damage or intravascular catheters. Antibiotics probably increase the incidence and extent of colonization and may play a role in increasing the risk of human infections.

In some cases of localized infection, the fungus may have seeded the site of infection directly. In patients with prosthetic valve endocarditis caused by Trichosporon spp, for example, there may have been direct infection of the prosthesis during the operative procedure rather than fungemia seeding the valve [31]. Other examples that may have resulted from direct inoculation of the fungus include:

Peritonitis in chronic ambulatory peritoneal dialysis [37-39]

Wound infections [40]

Meningitis following a myelogram [41]

Endophthalmitis after cataract surgery [42]

In vitro studies have shown that Trichosporon isolates are much more resistant to phagocytosis by neutrophils and monocytes than are isolates of Candida albicans [43,44]. Pretreatment with colony-stimulating factors and interferon-gamma did not enhance fungal killing by neutrophils but did increase killing by monocytes [43].

In experimental murine infections, intravenous injection of Trichosporon spp arthroconidia results in multiple focal abscesses throughout the body but especially in the kidneys [45]. Histologic inspection of lesions from both experimental and human infections shows that the formation of hyphae may assist in the invasion of tissues [46]. Emboli consisting of hyphae are frequently found occluding small blood vessels [46]. Many of the lesions in trichosporonosis are probably due to infarcts resulting from angioinvasive foci of Trichosporon spp.

Little is known about possible virulence traits in Trichosporon spp. Virulence factors such as toxins, special adherence properties, or components that allow the organism to evade the host's immune system have not yet been found. A cell wall antigen with similarities to the glucuronoxylomannan of Cryptococcus neoformans has been postulated to be a potential virulence factor [47].

CLINICAL PRESENTATIONS — As already mentioned, Trichosporon spp can cause both superficial and invasive infection.

Superficial infection — Patients with white piedra are usually asymptomatic and only seek medical attention because of the grossly visible nodules on the affected hair. Pruritus or pain at the involved site is an occasional complaint. The nodules are usually soft, pasty, and ivory colored. They are about 0.5 mm in size but can coalesce to blanket several millimeters of the hair shaft. Genital and facial hair are more often involved than the scalp and torso.

Invasive infection — Invasive infections due to T. asahii can be divided into disseminated and localized forms. The disseminated form is more common and, as mentioned above, usually occurs in neutropenic patients. The patient typically has an acute febrile illness that progresses rapidly to multiorgan failure.

Patients with pulmonary involvement can have dyspnea and a cough productive of scant, bloody sputum [48]. Chest radiographs usually show diffuse infiltrates with an alveolar pattern. Lobar infiltrates, reticulonodular infiltrates, and cavitation have also been observed. Patients with renal involvement usually have microscopic hematuria and proteinuria and progress to renal failure. Involvement of the kidneys has been nearly a universal finding in autopsies of patients with disseminated trichosporonosis.

Skin lesions are seen in about one-third of patients with disseminated trichosporonosis. The cutaneous manifestations include erythematous papules on the trunk and extremities that can sometimes form bullae [46,49,50]. Over time, the papules can develop central necrosis and appear as eschars.

Some patients who have recovered from their neutropenia and responded to antifungal drugs have presented with a chronic disseminated form of trichosporonosis that is similar to chronic hepatosplenic candidiasis. The few patients reported with this syndrome have had multiple lesions in the liver and spleen associated with fever and elevated serum alkaline phosphatase concentrations [23]. (See "Chronic disseminated candidiasis (hepatosplenic candidiasis)".)

Invasive Trichosporon spp infections less commonly can be confined to a single organ. The heart valves, central nervous system (CNS), peritoneum, and surgical wounds have all been described as involved sites in the absence of known infection elsewhere. Most of the cases of endocarditis due to Trichosporon spp have involved prosthetic valves [31,32,51]. However, there have been cases of native valve endocarditis in people who inject drugs. Valvular vegetations in Trichosporon endocarditis tend to be large and bulky as with other forms of fungal endocarditis. These vegetations have a predilection to embolize and cause sudden ischemic events, especially in the lower limbs [31,51].

In cases of CNS infection due to Trichosporon spp, the predominant symptoms are headache, nausea, vomiting, and fever [41,52]. Peritonitis with Trichosporon spp, as a complication of chronic ambulatory peritoneal dialysis, has also been described [37-39]. There are also increasing reports of bone involvement during dissemination of these fungi and, in particular, spine involvement such as spondylodiscitis [53].

Disseminated infections due to B. capitatus present in a fashion similar to those due to Trichosporon spp. Affected patients present with the sudden onset of fever and rapidly develop pulmonary abnormalities, hypotension, and renal failure. Some have had skin lesions with necrotic papules, and some have had CNS involvement with abscesses and meningitis [54].

DIAGNOSIS

Superficial infection — The diagnosis of white piedra is suggested by the characteristic nodules on the shafts of affected hairs. Examination of these nodules mounted on a slide with 10% potassium hydroxide shows septate hyphae with arthroconidia. Cultures of the nodules will grow Trichosporon spp in a few days.

Invasive infection — The culture of Trichosporon spp or B. capitatus from a sterile body site must always be regarded as indicative of invasive disease. In disseminated Trichosporon spp infections, cultures of blood, urine, sputum [48], cerebrospinal fluid (CSF) [52], and tissue have all yielded the fungus. Blood cultures are frequently positive in disseminated infection. Culture and histopathology of skin lesions have also been helpful in establishing the diagnosis in disseminated infections. Skin biopsies show dermal invasion by hyphae and arthroconidia, and some have shown thromboembolic vasculitis due to the fungi [46]. Bronchoscopy with bronchoalveolar lavage cultures can yield Trichosporon spp in patients with pneumonitis, and urine cultures have been positive in some cases of disseminated disease [48].

Mucosal, sputum, and urine cultures growing either Trichosporon spp or B. capitatus can represent colonization and need to be interpreted in the clinical context. However, in a neutropenic host, the culture of this organism from any specimen should be taken seriously and prompt further evaluation.

The diagnosis of disseminated trichosporonosis is occasionally suggested by a positive C. neoformans polysaccharide antigen assay due to cross-reactivity [10]. There have, however, been cases of disseminated trichosporonosis with negative cryptococcal antigen assays [27]; as a result, a negative test does not exclude trichosporonosis. CSF cryptococcal antigen assay, which was positive in one patient with meningitis caused by Trichosporon spp, may also be useful [52].

Blood cultures are positive in most cases of B. capitatus infection and establish the diagnosis of disseminated disease. Cultures of urine, sputum, and CSF [54] also may be positive in this setting. Cultures of skin biopsies appear to be positive less often in disseminated B. capitatus infections than in trichosporonosis. There are no specific serologic tests for this fungus, and there is no cross-reactivity with cryptococcal polysaccharide antigens.

TREATMENT

Superficial infection — The treatment of white piedra is best accomplished by shaving off all the hair in the affected areas and then applying a topical azole antifungal. The most commonly used regimen is 2% ketoconazole shampoo for 30 to 60 seconds once daily for several months, with the duration depending on the treatment response. For areas in which a shampoo might be irritating (eg, eyebrows, eyelashes), daily application of an azole antifungal cream for several months is an alternative. For the rare individual allergic to azoles, 6% precipitated sulfur in white petrolatum or 2% selenium sulfide foam may be substituted. If an individual refuses to shave the affected area, oral itraconazole (100 mg once daily for two to four months) should be added to the topical therapy.

Follow-up cultures are not routinely recommended but, when performed, they frequently remain positive despite clinical cure of the infection [21].

Invasive infection — The treatment of invasive infections due to either Trichosporon spp or B. capitatus is extremely difficult because of the profound immunosuppression and severe underlying diseases present in most infected patients. The optimal antifungal agent and duration of therapy are not known. Tentative recommendations can be made based on in vitro susceptibility data (table 1) and clinical experience.

In vitro susceptibility studies have shown that these two fungi are relatively resistant to most antifungal agents. Minimum inhibitory concentrations (MICs) to amphotericin B have ranged from 0.065 mcg/mL to >4 mcg/mL [3,23,48,55,56]. Strains of Trichosporon spp have been found to be inhibited but not killed by the concentrations of amphotericin B achievable in human serum [23].

The azole drugs fluconazole, itraconazole, posaconazole, voriconazole, and isavuconazole have shown activity against Trichosporon spp and B. capitatus in vitro [3,22,23,48,52,55-60]. When comparative in vitro studies for ranking azoles were done with T. asahii, voriconazole was the most active; itraconazole, posaconazole, and isavuconazole were less active than voriconazole but had similar levels of activity to one another; and fluconazole was the least active [61]. Some authors have recommended that voriconazole be considered the drug of choice for these infections [22,57,62,63]. However, as with amphotericin B, the achievable serum levels of these agents only result in inhibition rather than killing of these fungi.

Breakthrough infection has been described in patients receiving prophylactic amphotericin B, fluconazole, and voriconazole [24]. In one animal model of trichosporonosis, triazoles were more effective than amphotericin B [64]. Flucytosine has shown some synergistic activity against Trichosporon spp when combined with amphotericin B [23]. In vitro resistance to flucytosine has been reported in some strains.

The echinocandins are not active against Trichosporon spp. Several cases of invasive trichosporonosis have been reported in patients with hematologic malignancies receiving caspofungin or micafungin to prevent invasive aspergillosis and candidiasis in the setting of chemotherapy-induced neutropenia or hematopoietic cell transplantation [65,66].

Clinical experience in the treatment of trichosporonosis suggests that the drug used for treatment is probably not as important as the status of the underlying disease of the host. It is probable that no antifungal therapy will be effective with profound and prolonged neutropenia. In patients with disseminated infections due to Trichosporon spp or B. capitatus, we recommend initiating antifungal therapy with intravenous (IV) voriconazole (6 mg/kg IV every 12 hours for two doses, then 4 mg/kg IV twice daily) in combination with amphotericin B (a lipid formulation at 5 mg/kg IV daily or amphotericin B deoxycholate at 0.7 to 1.0 mg/kg IV daily); we prefer a lipid formulation of amphotericin B over amphotericin B deoxycholate since the former is associated with less nephrotoxicity and fewer infusion-related adverse effects.

Serum voriconazole trough concentrations should be checked four to seven days into therapy to ensure adequate dosing. Although debate remains over the optimal target concentration of voriconazole, available data suggest a therapeutic range of greater than 1 mg/L and less than 5.5 mg/L. (See "Pharmacology of azoles", section on 'Serum drug concentration monitoring'.)

There are no studies that have addressed the appropriate duration of combination therapy. After approximately one to two weeks of IV combination therapy, if the isolate is found to be susceptible to voriconazole and the patient is stable or improving, it is reasonable to switch to monotherapy with oral voriconazole (200 mg twice daily) with continued monitoring of serum levels as indicated.

At the same time that antifungal therapy is initiated, attention needs to be paid to the possibility of reversing any immunosuppressive conditions. Using stimulatory cytokines to increase neutrophil counts [67] or reducing the doses of glucocorticoids or other immunosuppressant medications are important factors in the treatment of these infections. Surgery appears to be indicated for those patients with local wound involvement or endocarditis. There is no experience with surgery for lung or brain lesions. Removal of IV catheters should be done in patients who have fungemia.

If the patient recovers, consideration should be given to maintaining chronic suppressive therapy since late relapses have occurred; oral voriconazole is the easiest agent to administer for this purpose. Chronic suppressive therapy is especially important for patients with endocarditis or central nervous system involvement. For patients with chronic immunosuppressive conditions, such as organ transplantation, therapy should probably be continued indefinitely.

Some patients will recover from their infections and will appear stable off antifungal therapy. If they subsequently become immunocompromised, as with repeat chemotherapy or antirejection therapy, systemic antifungal therapy should generally be restarted.

OUTCOMES — Invasive infections with Trichosporon spp and B. capitatus carry very high mortality rates. The only cures of infection have been seen in those patients who were either not neutropenic at the time of diagnosis or who recovered from their neutropenia quickly once the infection was diagnosed [55].

Occasional patients with endocarditis due to Trichosporon spp or B. capitatus have survived for a period of time. One patient with T. beigelii prosthetic valve infection lived for four years after two valve replacements and prolonged antifungal therapy but ultimately died of disseminated trichosporonosis [31]. Another patient with B. capitatus prosthetic valve infection died two months after diagnosis despite two additional valve replacements and antifungal therapy with amphotericin B and flucytosine [12].

Patients with localized disease, such as wound infections or cellulitis due to T. beigelii, have apparently been cured with surgical debridement and prolonged antifungal therapy [40,55]. Some patients with positive blood cultures for T. beigelii have also been apparently cured of infection. Examples include a patient with Trichosporon fungemia thought to be due to injection drug use [68] and a non-neutropenic patient with extensive burns who had fungemia [27]. In another report, a 14-year-old patient who had undergone an allogeneic bone marrow transplant for acute lymphoid leukemia was diagnosed with central nervous system involvement due to B. capitatus and survived for more than one year on antifungal therapy with resolution of her symptoms [54]. When she subsequently died of interstitial pneumonia, residual fungal infection was found in the meninges at autopsy.

SUMMARY AND RECOMMENDATIONS

MycologyTrichosporon species and Blastoschizomyces capitatus are related fungi and are rare causes of invasive infection in humans. Trichosporon spp can be found as a constituent of normal flora but can also cause both superficial and invasive infections in humans.

Epidemiology − Invasive disease due to Trichosporon spp occurs almost exclusively in immunocompromised hosts, appears to be increasing in frequency, and is usually fatal. The most common species to cause invasive infection is Trichosporon asahii. The majority of trichosporonosis cases have been seen in patients with hematologic malignancies, often in the setting of neutropenia. This fungus also causes a characteristic infection of hair shafts called white piedra. B. capitatus has only been described as a systemic pathogen, and almost all of the affected patients have had some underlying immunocompromising condition, usually neutropenia. (See 'Epidemiology' above.)

Superficial infections

Clinical presentation − White piedra occurs primarily in immunocompetent patients in tropical climates but also occurs in some temperate regions. Patients with white piedra are usually asymptomatic and only seek medical attention because of the grossly visible nodules on the affected hair. (See 'Superficial infection' above.)

Diagnosis − The diagnosis of white piedra is suggested by the characteristic nodules on the shafts of affected hairs. Examination of these nodules mounted on a slide with 10% potassium hydroxide shows septate hyphae with arthroconidia. Cultures of the nodules will grow Trichosporon spp in a few days. (See 'Superficial infection' above.)

Treatment − The treatment of white piedra is best accomplished by shaving off all the hair in the affected areas and then applying a topical azole antifungal such as 2% ketoconazole shampoo for several months. (See 'Superficial infection' above.)

Invasive infections

Clinical manifestations − Invasive infections due to Trichosporon species can be divided into disseminated and localized forms. The disseminated form is more common; the patient typically has an acute febrile illness that progresses rapidly to multiorgan failure. Disseminated infections due to B. capitatus present in a fashion similar to those due to Trichosporon spp. (See 'Clinical presentations' above.)

Diagnosis − In disseminated Trichosporon spp infections, cultures of blood, urine, sputum, cerebrospinal fluid, and tissue have all yielded the fungus. Blood cultures are frequently positive in disseminated infection. Culture and histopathology of skin lesions have also been helpful in establishing the diagnosis in disseminated infections. (See 'Invasive infection' above.)

Treatment

-The treatment of invasive infections due to either Trichosporon spp or B. capitatus is extremely difficult because of the profound immunosuppression and severe underlying diseases present in most infected patients. The optimal antifungal agent and duration of therapy are not known, but tentative recommendations can be made based on in vitro susceptibility data (table 1) and clinical experience. (See 'Invasive infection' above.)

-In patients with disseminated infections due to Trichosporon spp or B. capitatus, we recommend initiating antifungal therapy with intravenous (IV) voriconazole (6 mg/kg IV every 12 hours for two doses, then 4 mg/kg IV twice daily) in combination with amphotericin B (a lipid formulation at 5 mg/kg IV daily or amphotericin B deoxycholate at 0.7 to 1.0 mg/kg IV daily); we prefer a lipid formulation of amphotericin B over amphotericin B deoxycholate since the former is associated with less nephrotoxicity and fewer infusion-related adverse effects. (See 'Invasive infection' above.)

Outcomes − Invasive infections with Trichosporon spp and B. capitatus carry very high mortality rates. The only cures of infection have been seen in those patients who were either not neutropenic at the time of diagnosis or who recovered from their neutropenia quickly once the infection was diagnosed. (See 'Outcomes' above.)

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Topic 2456 Version 33.0

References

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