Next Article in Journal
Sordariomycetes Taxa Associated with Dracaena in Karst Outcrops: Two Novel Species and Five New Host Records from Thailand
Previous Article in Journal
Morphological Diversity of Epichloë sinensis from Festuca sinensis Germplasm on the Qinghai–Tibet Plateau
Previous Article in Special Issue
Breaking the Chain of Infection: A Systematic Review of Environmental Decontamination of Candidozyma auris (2017–2025)
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

Trichosporonaceae as (Re-)Emerging Pathogens: A Warning to the Medical Community

by
Yasmim Passos Lima
1,
Ricardo Villela Bastos
2,
Victor Quinet de Andrade Bastos
2,
Lucas Quinet de Andrade Bastos
2,
João Renato Hipólito
2,
André Netto Bastos
3,
Cláudio Galuppo Diniz
4,
Vania Lucia Da Silva
4 and
Vanessa Cordeiro Dias
4,*
1
Graduate Program in Biological Science, Federal University of Juiz de Fora—UFJF, Rua José Lourenço Kelmer, s/n, São Pedro, Juiz de Fora, MG 36036 900, Brazil
2
Cortes Villela Laboratory, Avenida Barão do Rio Branco, 2406/4 andar, Juiz de Fora, MG 36016 904, Brazil
3
Department of Morphology, Federal University of Juiz de Fora—UFJF, Rua José Lourenço Kelmer, s/n, São Pedro, Juiz de Fora, MG 36036 900, Brazil
4
Department of Parasitology, Microbiology, and Immunology, Federal University of Juiz de Fora—UFJF, Rua José Lourenço Kelmer, s/n, São Pedro, Juiz de Fora, MG 36036 900, Brazil
*
Author to whom correspondence should be addressed.
J. Fungi 2026, 12(3), 167; https://doi.org/10.3390/jof12030167
Submission received: 9 January 2026 / Revised: 10 February 2026 / Accepted: 17 February 2026 / Published: 26 February 2026
(This article belongs to the Special Issue Advances and Innovations in Fungal Infections)

Abstract

Background: The Trichosporonaceae family includes genera such as Trichosporon, Apiotrichum, and Cutaneotrichosporon, which are components of the human microbiota but may cause infections under conditions such as immunosuppression, prolonged hospitalization, invasive procedures, and broad-spectrum antimicrobial use. Objectives: This study aimed to describe the clinical and epidemiological characteristics of hospitalized and outpatient individuals with positive cultures for Trichosporonaceae species in Juiz de Fora, Minas Gerais, Brazil, and to correlate these findings with antifungal susceptibility profiles. Methods: Clinical isolates collected between 2020 and 2023 were identified using the Vitek 2® system, and antifungal susceptibility was assessed by disk diffusion. Clinical and epidemiological data were obtained from electronic health records. Results: Among 40 isolates, Trichosporon asahii predominated (92.5%). Most cases involved hospitalized individuals (83.8%), mainly from intensive care units (81.8%). Respiratory infections and acute renal failure were the most common reasons for admission. The mean hospital stay was 34.8 days, and overall mortality reached 51.6%. Most individuals were male (77.5%) and older than 61 years (57.5%). Urine was the most frequent specimen (52.5%), and invasive infections predominated (87.5%). Corticosteroid use and invasive devices were common, and prior antibiotic use occurred in most cases. Only 35.0% of patients received antifungal therapy, predominantly fluconazole. Conclusions: Trichosporonaceae infections, particularly those caused by T. asahii, are associated with critically ill patients and high mortality, highlighting the need for early diagnosis, appropriate therapy, and continuous surveillance.

1. Introduction

The order Trichosporonales (phylum Basidiomycota, class Tremellomycetes) encompasses a diverse group of yeast-forming fungi, some of which have gained increasing recognition as opportunistic human pathogens of clinical relevance [1]. The Trichosporonaceae family consists of genera such as Trichosporon, Apiotrichum, Cutaneotrichosporon, Effuseotrichosporon, and Haglerozyma. Recent taxonomic re-evaluations have identified new genera. Various species have been shown to possess pathogenic potential and virulence factors, especially in clinical isolates [2].
Among the most frequently reported species within the genera comprising the Trichosporonaceae family are Trichosporon (including Trichosporon asahii, Trichosporon inkin, Trichosporon ovoides, Trichosporon asteroides, Trichosporon coremiiforme, Trichosporon faecale, Trichosporon japonicum, Trichosporon lactis, and Trichosporon dohaense), Apiotrichum (including Apiotrichum mycotoxinivorans, Apiotrichum domesticum, Apiotrichum montevideense, and Apiotrichum loubieri), Cutaneotrichosporon (including Cutaneotrichosporon dermatis, Cutaneotrichosporon cutaneum, Cutaneotrichosporon jirovecii and Cutaneotrichosporon mucoides), Effuseotrichosporon (Effuseotrichosporon vanderwaltii) and Haglerozyma (Haglerozyma chiarellii) [2].
These fungi show characteristic macromorphology when grown on Sabouraud Dextrose Agar (SDA). They usually form dry, cerebriform colonies in white, beige, or cream colors [3,4]. Microscopically, they exhibit yeast-like structures, including blastoconidia, pseudohyphae, and arthroconidia. Arthroconidia are a distinctive trait of Trichosporon spp. [5,6] (Figure 1).
While morphological characteristics are useful, identifying Trichosporon species with conventional methods is often challenging and often yields inconclusive results. This difficulty is compounded by the absence of standardized in vitro susceptibility testing protocols [7]. Consequently, as observed with other fungal genera, molecular techniques are now recommended for the accurate identification of yeast species formerly classified under the genus Trichosporon. Taxonomic revisions have led to the reclassification of several clinically relevant species into three distinct genera: Trichosporon, Apiotrichum, and Cutaneotrichosporon [2].
These fungi are part of the healthy human microbiota and colonize the skin, nails, hair, and the respiratory and gastrointestinal tracts, as well as mucosal surfaces, albeit transiently. They are also present in a variety of environmental reservoirs, including soil, water, decomposing wood, and bird and bat droppings [8]. These yeasts can act as opportunistic pathogens in the presence of predisposing factors such as immunosuppression, prolonged hospitalization, invasive procedures, or the use of broad-spectrum antimicrobials [5,9].
Superficial infections caused by Trichosporonaceae such as white piedra, a benign, chronic condition characterized by irregular, light-colored nodules along the hair shaft composed of blastoconidia, pseudo-hyphae, and arthroconidia, are relatively common, especially in immunocompetent hosts. Other cutaneous manifestations include dermatitis and onychomycoses [5,10].
Invasive infection, though less frequent than superficial manifestations, is a significant clinical concern due to high morbidity and mortality. These infections mainly affect hospitalized or critically ill individuals. Those with hematologic malignancies, organ dysfunction, or in intensive care units (ICUs) are at higher risk [11,12]. The growing incidence is linked to an increasing number of immunocompromised patients. Many undergo chemotherapy, immunosuppressive therapies, broad-spectrum antibiotics, invasive procedures, or solid organ transplantation. These conditions increase susceptibility and lead to poor clinical outcomes [1,7].
These infections are associated with high morbidity and mortality, representing a considerable challenge due to the limited therapeutic arsenal [13]. Currently, voriconazole is recommended as the first-line treatment based on in vitro sensitivity data, which also highlight posaconazole as an effective option against clinical isolates of Trichosporon spp. [14,15]. More recently, isavuconazole has gained prominence as a valuable alternative to voriconazole, offering a comparable antifungal spectrum with fewer drug interactions, reduced adverse effects, and predictable pharmacokinetics [16,17]. Amphotericin B and fluconazole may also be used, often in combination therapy, depending on the clinical scenario [18]. Treatment duration typically extends for 14 days in superficial infections, with longer courses required for invasive cases, particularly in immunocompromised individuals due to the high mortality rates [15].
The epidemiological distribution of clinically relevant Trichosporon species was assessed in a Brazilian population comprising 112 individuals. The species most frequently isolated from normal perigenital skin was C. cutaneum (29.46%), followed by T. inkin (10.71%). C. mucoides (8.92%) and T. asahii (6.25%) were also detected. Skin colonization was more prevalent among individuals aged 21–30 years (48.2%) and 31–40 years (25.0%). In clinical samples from urine and catheters, T. asahii was the predominant species (76.5%; n = 23), followed by T. inkin (16.6%; n = 5). The highest frequency of isolates from these samples was observed in the 71–80 age group (36.7%), followed by individuals aged 61–70 years (26.7%) [2,19].
With the recognition of Trichosporonaceae as emerging pathogens, it is vital to understand their clinical relevance, distribution, and antifungal susceptibility. Therefore, this study aimed to describe the clinical and epidemiological characteristics of hospitalized and non-hospitalized individuals with cultures positive for Trichosporonaceae species in Juiz de Fora, Minas Gerais, Brazil, between 2020 and 2023, and to correlate these findings with the antifungal susceptibility profiles of the isolates. This approach may support early recognition of infection, guide therapeutic decisions, and enhance the surveillance of these microorganisms.

2. Material and Methods

This was an experimental, descriptive, and cross-sectional study involving 40 unique clinical isolates of Trichosporonaceae, collected from hospitalized or non-hospitalized individuals. The samples were obtained from a clinical microbiology laboratory located in Juiz de Fora, Minas Gerais, Brazil, over a period from January 2020 to December 2023.
The participating institution is a private hospital with an approximate capacity of 160 beds and includes various specialized units, such as neonatal and adult intensive care units, coronary and neurological wards, surgical and general medical departments, and outpatient services.
All procedures were performed in accordance with ethical guidelines, following approval from the Human Research Ethics Committee of the Federal University of Juiz de Fora (CAAE 18611019.6.0000.5147) and after obtaining informed consent from all participants.

2.1. Study Participants

The inclusion criteria encompassed individuals with laboratory-confirmed positive cultures for Trichosporonaceae, irrespective of demographic variables such as age, sex, or unit origin (hospitalized or non-hospitalized). To prevent duplication, repeated isolates from the same individual were excluded from the analysis.

2.2. Review of Medical Records

An analysis of electronic medical records was conducted for individuals with Trichosporonaceae isolates. The variables extracted included: age, sex, unit of origin (hospitalized or non-hospitalized), inpatient unit, length of hospital stay, reason for hospitalization, clinical specimen, previous use of antimicrobials, use of antifungals after the diagnosis, use of corticosteroids within the 30 days prior to fungal culture testing, use of invasive devices, risk factors, and clinical outcome. All information was recorded and organized in a digital spreadsheet for further analysis (Excel® version 2023).

2.3. Fungal Culture

Clinical specimens were inoculated onto Sabouraud Dextrose agar (Neogen of Brazil, Lansing, MI, USA), according to recommendations [19], and incubated at 35 °C for up to 30 days. After, the fungal isolates were preserved in sterile 2 mL tubes containing sterile distilled water, following the method outlined by Diogo et al. (2005) [20].
Morphological examinations and Gram staining were performed to evaluate the growth, viability, and purity of the isolates.

2.4. Yeast Identification

Yeast isolates were identified through biochemical and physiological analyses using the Vitek 2® automated system (bioMérieux, Marcy-l’Étoile, France), as recommended by the manufacturer.
The reference strain T. asahii ATCC 90039 (American Type Culture Collection, Manassas, VA, USA) was used as quality control, yielding a 99.9% identification match, thus confirming the system’s reliability.

2.5. Susceptibility Testing to Antifungal Agents

The susceptibility profile of the Trichosporonaceae isolates was determined based on the guidelines established by the Clinical and Laboratory Standards Institute (CLSI) [21]. Antifungal susceptibility was evaluated using the disk diffusion method, with the following antifungal agents, fluconazole (25 μg), voriconazole (1 μg), amphotericin B (20 μg), and caspofungin (5 μg), all provided by Liofilchem Diagnostics (Roseto degli Abruzzi, Italy).
Each test was performed in duplicate, including controls for each antifungal. After incubation at 35 °C for 24 h, the diameter of the inhibition zones surrounding each disk was measured.
The interpretive criteria followed those proposed by Pfaller et al. (2010) [22] for fluconazole and voriconazole, Menezes et al. (2012) [23] for amphotericin B, and the manufacturer’s specifications (Liofilchem et al., 2021) [24] and CLSI [25] for caspofungin.

2.6. Statistical Analysis

Descriptive statistical analysis was performed, including percentages, absolute frequency, range, and mean values for participant age. Statistical analyses were performed using bivariate methods. Categorical variables were compared using Fisher’s exact test due to small sample size and expected frequencies below five. Continuous variables were compared using the Mann–Whitney U test after assessment of non-normal distribution. A p-value < 0.05 was considered statistically significant.

3. Results

A total of 40 Trichosporonaceae isolates were recovered, predominantly from hospitalized individuals (n = 33/82.5%). Most cases occurred in male individuals (n = 31/77.5%) and individuals older than 61 years (n = 23/57.5%) (Figure 2).
Among the individuals infected by T. asahii, the most frequent species in this study, it mainly affected hospitalized elderly (n = 22/59.5%) and males (n = 29/78.9%). The two cases involving C. mucoides occurred in hospitalized male individuals: one adult and one elderly. T. inkin isolate was detected in a non-hospitalized adult male (Figure 2).
Defining invasive infection as that resulting from deep tissue penetration (e.g., urinary or respiratory tract) or hematogenous dissemination, most cases in this study met these criteria (n = 35/87.5%), with a mean hospital stay of 34.8 days (range: 1–102). Among individuals with available clinical data, most were admitted to intensive care units, particularly neurological ICUs (n = 11/33.3%). The most frequent causes of hospitalization were respiratory infection (n = 8/24.2%) and acute renal failure (n = 7/21.2%). Overall mortality reached 51.5% (n = 17). Prior corticosteroid exposure was reported in 63.6% (n = 21) of cases, and risk factors such as invasive procedures were observed in 37.5% (n = 15) of individuals (Table 1).
Urine was the most common clinical specimen (n = 21/52.5%), followed by bronchoalveolar lavage (n = 11/27.5%). All hospitalized individuals required invasive medical devices, and most individuals were exposed to multiple devices, reflecting the high clinical complexity of this study (Figure 3).
Prior antimicrobial exposure was observed in 72.5% (n = 29) of individuals, with combination therapy being the most common regimen (n = 24/60.0%). Following fungal diagnosis, only 35% (n = 14) of individuals received antifungal therapy, predominantly fluconazole (n = 7/17.5%). Notably, 65.0% (n = 26) of individuals did not receive any antifungal agents following diagnosis, underscoring potential gaps in targeted therapeutic management (Table 2).
To further evaluate potential clinical factors associated with unfavorable outcomes, a statistical analysis was performed comparing survivors and non-survivors among individuals with available clinical outcome data (n = 33). This analysis was conducted to identify variables potentially associated with mortality and is summarized in Table 3.
ICU admission was strongly associated with mortality, occurring in 88.2% of individuals who died compared to 18.7% of survivors (p < 0.001; OR 32.5; 95% CI 4.3–245.0). Prior antimicrobial exposure and previous corticosteroid therapy were also significantly associated with death (p = 0.018 and p = 0.004, respectively). Individuals who died were significantly older and had longer hospital stays (p = 0.004 and p = 0.040, respectively). Although antifungal therapy after diagnosis was more frequent among individuals who died, this association did not reach statistical significance (p = 0.080).
All C. mucoides and T. inkin isolates were susceptible to fluconazole, voriconazole, and amphotericin B. Among T. asahii isolates, full susceptibility to azoles was observed, whereas resistance to amphotericin B was detected in four isolates (Graph 1).
Graph 1. In vitro sensitivity of Trichosporonaceae isolates to antifungal agents.
Graph 1. In vitro sensitivity of Trichosporonaceae isolates to antifungal agents.
Jof 12 00167 gr001

4. Discussion

The present study provides clinical and epidemiological insights into Trichosporonaceae infections and identifies factors associated with mortality. T. asahii was the predominant species (92.5%), reinforcing its role as the most clinically relevant member of the genus, particularly in hospitalized and immunocompromised individuals. This predominance is consistent with previous studies describing T. asahii as the main etiological agent of invasive trichosporonosis [26,27]. Although less frequent, C. mucoides and T. inkin remain clinically relevant species and should not be overlooked, especially in specific clinical contexts [2,28].
The species identified in the present study are considered among the most clinically relevant in this genus [2,29]. The identification of T. inkin in a nail scraping specimen reinforces the role of this species in superficial infections, as described in studies associating it with white piedra, onychomycosis, and dermatomycoses [28,30,31]. These findings highlight the clinical diversity of Trichosporonaceae infections, which may range from superficial colonization to potentially fatal invasive disease.
The clinical profile observed in this study, characterized by a predominance of elderly male individuals, is consistent with previous reports of a higher susceptibility to opportunistic yeast infections in these populations. This distribution may be explained by the higher burden of comorbidities and immunosuppressive conditions commonly observed among elderly males, including malignancies, chronic renal disease, and diabetes mellitus, as well as age-related immune dysfunction (immunosenescence) [26,27]. In addition, sex-related immunological differences and increased exposure to invasive procedures, prolonged hospitalization, and indwelling medical devices in this group may further contribute to the increased risk of infection, reinforcing the role of host-related factors in the epidemiology of Trichosporon spp. infections [32,33].
Advanced age and longer hospital stay were also associated with mortality, reinforcing the role of host vulnerability and prolonged healthcare exposure in unfavorable outcomes.
The urinary tract was the main site of fungal isolation, particularly among hospitalized individuals undergoing urinary catheterization. This finding reinforces the urinary tract as an important reservoir for Trichosporon spp., especially in individuals with invasive devices [33,34,35]. Similar trends were found in a retrospective cohort from Mexico City (2019–2023), which identified 26 cases of T. asahii from urine cultures, mostly in male individuals (73%), all with urinary catheters, and the majority with central venous catheters (96%) and ICU admission (70%) [33]. Likewise, at King Abdulaziz University Hospital in Saudi Arabia, T. asahii accounted for 90.5% of Trichosporon isolates, with urinary tract infections predominating among elderly men [27].
In this study, we identified three individuals aged between birth and two years old. In early life, the gut mycobiome undergoes significant changes influenced by factors such as mode of delivery and exposure to intrapartum antibiotics. One study found that Trichosporon became the dominant fungal genus by 18 months of age, especially in vaginally delivered infants exposed to antibiotics during labor, where it accounted for up to 66% of the fungal community. These findings suggest that antibiotic exposure, although not directly affecting fungi, may alter fungal populations by altering the bacterial microbiota [36].
In the context of the human microbiota, this study’s results provide important insights into the relationship between fungal species and the presence of invasive devices, which can alter the host’s microbiological dynamics. The most frequent clinical sample in this study was urine, suggesting that fungal colonization of the urinary tract may be associated with invasive devices, such as peripheral catheters, central venous catheters, enteral tubes, and urinary catheters, which were the most commonly used in our study. Furthermore, the alteration of the microbiota caused by the presence of these devices may create an environment conducive to the proliferation of opportunistic fungi, which, by invading tissues or internal systems, can lead to severe infections, such as fungemia or urinary tract infections, especially in immunocompromised patients or those with predisposing conditions [37].
This risk is even more pronounced in ICUs, where individuals present greater immunological vulnerability and are exposed to various invasive medical devices [38]. The ability of fungi to survive for extended periods on inert surfaces, combined with the difficulty of removing them and the lack of effective, continuous disinfection practices, underscores the need for rigorous environmental surveillance and effective control strategies, particularly in critical areas such as ICUs [39,40].
The infectious picture is aggravated by the widespread ability of Trichosporonaceae, especially Trichosporon spp., to form biofilms, mainly in medical devices such as central venous catheters, urinary catheters, and cardiac implants [41,42]. These biofilms offer protection against antifungal agents and immune responses, promoting persistence and recurrence [5,43,44].
Prior antimicrobial exposure was also significantly associated with mortality. Broad-spectrum antimicrobial therapy may disrupt normal microbiota, promoting colonization and dissemination of opportunistic fungi. This finding reinforces the importance of antimicrobial stewardship and microbiological surveillance in hospital environments [36,37].
Prior corticosteroid use was reported in 63.6% of cases, highlighting its relevance as an important predisposing factor for opportunistic fungal infections [45]. In the present study, corticosteroid therapy was also significantly associated with mortality, reinforcing its clinical impact on disease outcomes. Corticosteroids impair both innate and adaptive immune responses by reducing neutrophil and macrophage function, inhibiting cytokine production, and suppressing T-cell-mediated immunity, which are essential mechanisms for controlling opportunistic yeasts [46]. Additionally, prolonged or high-dose corticosteroid therapy may disrupt mucocutaneous barriers and alter host microbiota, facilitating fungal colonization and subsequent invasion. In the context of Trichosporon spp. infections, prior corticosteroid exposure has been frequently associated with severe disease and unfavorable outcomes, particularly among elderly and immunocompromised patients, emphasizing the importance of careful risk assessment and early recognition of invasive fungal infections in this population [47,48].
Despite microbiological confirmation of infection, antifungal therapy was administered in only 35% of cases, revealing an important gap between laboratory diagnosis and clinical management. This discrepancy underscores a disconnect between laboratory diagnosis and clinical intervention. Considering the high mortality rate, one must question whether more assertive and timely use of antifungal agents could have improved patient survival. This finding serves as a critical warning and reinforces the urgent need for early therapeutic decisions aligned with microbiological findings in the management of invasive fungal infections.
Although antifungal therapy was more frequently administered to individuals who died, no statistically significant association with mortality was observed. This finding likely reflects confounding by indication, since antifungal treatment is more commonly initiated in patients with more severe clinical conditions. Additionally, the high proportion of patients who did not receive antifungal therapy after fungal isolation may reflect challenges in differentiating colonization from invasive infection and highlights potential gaps in therapeutic decision-making.
T. asahii has emerged as the most frequently reported pathogen among rare yeast infections in Latin America, accounting for 49.5% of the 495 cases reviewed across eight countries [49]. These infections are associated with severe clinical outcomes, including a crude mortality rate of 40.8%, which increases significantly in cases of fungemia. The affected population is predominantly male and spans a wide age range from neonates to the elderly, highlighting the opportunistic potential of this pathogen. In addition, prior surgical procedures and antibiotic use have been statistically linked to an increased incidence of Trichosporon infections, reinforcing the importance of the hospital environment as a key setting for disease acquisition [49].
These findings highlight the urgent need for enhanced diagnostic vigilance and effective therapeutic strategies, given the persistently high lethality of T. asahii, even in individuals treated with antifungal agents such as amphotericin B [23].
In this research, antifungal sensitivity was assessed using the disk diffusion method, focusing on key agents such as fluconazole, voriconazole, and amphotericin B. Despite its limited standardization by major regulatory bodies, this method is recognized for its simplicity, reproducibility in routine laboratory settings, and low cost. Although its use remains underreported in scientific studies, especially in studies of Trichosporonaceae, it offers a wide range of potential clinical applications.
Among treated individuals, azole derivatives were the most frequently prescribed antifungals. Although Trichosporon spp. generally demonstrates susceptibility to this class, therapeutic failures may occur due to biofilm formation, host-related factors, and pharmacological limitations of antifungal agents. In contrast, combination therapy, especially when associated with polyenes, showed better outcomes, as three of the four discharged individuals were on combined regimens with other antifungal classes, suggesting potential benefits of synergistic antifungal approaches.
Azole derivatives inhibit ergosterol biosynthesis at the plasma membrane, thereby altering membrane permeability and enzyme function [50]. Clinical isolates of Trichosporon are generally susceptible to azoles, but multi-resistant strains have already been reported [51].
Antifungal agents from the echinocandin class show limited activity against Trichosporon spp. because these fungi have low levels of 1,3-β-D-glucan in their cell walls, the primary target of echinocandins. As a result, echinocandins exhibit poor fungistatic or fungicidal effects against Trichosporon, making them ineffective in clinical practice [3,52]. For this reason, they are not recommended for the treatment of invasive trichosporonosis, and alternative antifungals such as azoles (e.g., voriconazole) should be used [3,52].
Polyene antifungals exert their effect by extracting ergosterol from fungal membranes, forming so-called “ergosterol sponges” that disrupt membrane integrity. These agents have both fungistatic and fungicidal activity [53]. However, studies have shown that T. asahii is not only intrinsically resistant to caspofungin but also exhibits greater resistance to amphotericin B than other Trichosporon species. Resistance to amphotericin B and caspofungin is particularly concerning, as these are among the most widely used systemic antifungals in clinical practice, especially as first-line agents in the treatment of yeast infections [54].
Laboratory antifungal susceptibility testing is crucial, as empirical use of commonly prescribed agents, such as echinocandins, may result in therapeutic failure. Antifungal selection should therefore be guided by microbiological and susceptibility data to improve treatment outcomes, reduce healthcare costs, and minimize mortality.
It is important to emphasize that isolation of Trichosporon spp., particularly from urine samples, does not necessarily indicate causality in fatal outcomes. Many individuals in this cohort presented severe underlying diseases and multiple risk factors for mortality. Due to the retrospective design and limited clinical data, attributable mortality could not be determined, and findings should therefore be interpreted as associations between fungal isolation and unfavorable outcomes rather than confirmation of causality.
Ongoing surveillance of antifungal sensitivity patterns is essential not only to guide effective therapy but also to prevent the emergence of resistant strains [10,55] and to support the development of new antifungal agents. The findings of this study reinforce the concern that delays in the clinical response to laboratory diagnoses may negatively influence outcomes, particularly among vulnerable patient populations [8,14,56].
On the other hand, although the increasing number of reported cases of infections caused by Trichosporonaceae species represents a significant clinical challenge, it also opens avenues for innovation. There is a clear need for ongoing research into new antifungal compounds and the improvement in existing ones, the refinement of laboratory diagnostic methods, and hospital protocols that prioritize early recognition and targeted therapy. Addressing these gaps is essential for reducing the mortality and morbidity associated with this emerging group of opportunistic pathogens. Finally, raising awareness about fungi is important [57,58].
This study provides real-world data on Trichosporonaceae infections, highlighting their occurrence in both community and hospital settings and their association with critically ill patients and high mortality. The integration of clinical, epidemiological, and antifungal susceptibility data strengthens the relevance of the findings and underscores important gaps in diagnosis and treatment, particularly the low rate of antifungal therapy after diagnosis. However, the small sample size, incomplete clinical data, and reliance on disk diffusion for antifungal susceptibility testing may limit the generalizability of the results. Despite these limitations, this study offers valuable insights into the clinical burden and therapeutic challenges posed by Trichosporonaceae infections, reinforcing the need for improved surveillance, early diagnosis, and timely antifungal management.

5. Conclusions

Infections caused by Trichosporonaceae represent a significant challenge in hospital settings due to their high lethality and frequent association with critically ill individuals. The findings of this study highlight the circulation of these fungi both in the community and within hospital environments, underscoring the need for enhanced clinical and laboratory surveillance. The high mortality rate observed among hospitalized individuals reinforces the severity of these infections. Although Trichosporonaceae isolates show good sensitivity to fluconazole and voriconazole, intrinsic resistance to caspofungin underscore the complexity of therapeutic management.
Additionally, the identification of a significant therapeutic gap, in which only 35% of individuals received antifungal treatment after diagnosis, reveals an important area for improvement in clinical care. The high proportion of individuals untreated with antifungals, combined with diagnostic delays and a lack of clinical suspicion, may have contributed to the unfavorable outcomes observed. These findings highlight the urgent need to raise awareness among healthcare professionals and implement standardized protocols for the timely initiation of appropriate antifungal therapy.

Author Contributions

Y.P.L.: Conceptualization, Formal analysis, Investigation, Resources, Writing—Review and Editing. R.V.B.: Conceptualization, Formal analysis, Investigation, Resources, Writing—Review and Editing. V.Q.d.A.B.: Conceptualization, Formal analysis, Investigation, Resources, Writing—Review and Editing. L.Q.d.A.B.: Conceptualization, Formal analysis, Investigation, Resources, Writing—Review and Editing. J.R.H.: Conceptualization, Formal analysis, Investigation, Resources, Writing—Review and Editing. A.N.B.: Conceptualization, Formal analysis, Investigation, Resources, Writing—Review and Editing. C.G.D.: Conceptualization, Formal analysis, Investigation, Resources, Writing—Review and Editing. V.L.D.S.: Conceptualization, Formal analysis, Investigation, Resources, Writing—Review and Editing. V.C.D.: Conceptualization, Formal analysis, Investigation, Resources, Writing—Review and Editing, and Supervision. All authors have read and agreed to the published version of the manuscript.

Funding

The authors would like to acknowledge the UFJF, CAPES, PPGCBIO (Graduate Program in Biological Sciences), FAPEMIG (APQ-00995-25), and Cortes Villela Laboratory.

Institutional Review Board Statement

This study was reviewed and approved by the Research Ethics Committee of the Federal University of Juiz de Fora (CEP/UFJF), Brazil. All methods were carried out in accordance with relevant institutional guidelines and regulations.

Data Availability Statement

All data generated or analyzed during this study on Trichosporon spp. are included in this published article.

Conflicts of Interest

The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

References

  1. do Espírito Santo, E.P.T.; Monteiro, R.C.; da Costa, A.R.F.; Marques-da-Silva, S.H. Molecular Identification, Genotyping, Phenotyping, and Antifungal Susceptibilities of Medically Important Trichosporon, Apiotrichum, and Cutaneotrichosporon Species. Mycopathologia 2019, 185, 307–317. [Google Scholar] [CrossRef]
  2. Liu, X.Z.; Wang, G.M.; Göker, M.; Groenewald, M.; Kachalkin, A.V.; Lumbsch, H.T.; Millanes, A.M.; Wedin, M.; Yurkov, A.M.; Boekhout, T.; et al. Towards an integrated phylogenetic classification of the Tremellomycetes. Stud. Mycol. 2015, 81, 85–147. [Google Scholar] [CrossRef]
  3. Chagas-Neto, T.C.; Chaves, G.M.; Colombo, A.L. Update on the genus Trichosporon. Mycopathologia 2008, 166, 121–132. [Google Scholar] [CrossRef]
  4. Lara, B.R.; de Camargo, B.B.; Paula, C.R.; Junior, D.P.L.; Garces, H.G.; Arnoni, M.V.; Silveira, M.; Gimenes, V.M.F.; Siqueira, L.P.M.; Takahashi, J.P.F.; et al. Comparing the phenotypic, genotypic, and proteomic identification of Trichosporon species: A globally emerging yeast of medical importance. Med. Mycol. 2021, 59, 1181–1190. [Google Scholar] [CrossRef]
  5. Colombo, A.L.; Padovan, A.C.; Chaves, G.M. Current knowledge of Trichosporon spp. and Trichosporonosis. Clin. Microbiol. Rev. 2011, 24, 682–700. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  6. Matsumoto, Y.; Yoshikawa, A.; Nagamachi, T.; Sugiyama, Y.; Yamada, T.; Sugita, T. A critical role of calcineurin in stress responses, hyphal formation, and virulence of the pathogenic fungus Trichosporon asahii. Sci. Rep. 2022, 12, 16126. [Google Scholar] [CrossRef]
  7. Chagas-Neto, T.C.; Chaves, G.M.; Melo, C.O.M.O.; Colombo, A.L. Bloodstream infections due to Trichosporon asahii genotypes determined on the basis of ribosomal DNA intergenic spacer 1 sequencing, and antifungal susceptibility testing. J. Clin. Microbiol. 2009, 47, 1074–1081. [Google Scholar] [CrossRef] [PubMed]
  8. Guo, L.N.; Yu, S.Y.; Hsueh, P.R.; Al-Hatmi, A.M.S.; Meis, J.F.; Hagen, F.; Xiao, M.; Wang, H.; Barresi, C.; Zhou, M.L.; et al. Invasive Infections due to Trichosporon: Species Distribution, Genotyping, and Antifungal Susceptibilities from a Multicenter Study in China. J. Clin. Microbiol. 2019, 57, e01505-18. [Google Scholar] [CrossRef] [PubMed]
  9. Lee, E.H.; Choi, M.H.; Lee, K.H.; Song, Y.G.; Han, S.H. Differences of clinical characteristics and outcome in proven invasive Trichosporon infections caused by asahii and non-asahii species. Mycoses 2023, 66, 992–1002. [Google Scholar] [CrossRef]
  10. Mehta, V.; Nayyar, C.; Gulati, N.; Singla, N.; Rai, S.; Chandar, J. A Comprehensive Review of Trichosporon spp.: An Invasive and Emerging Fungus. Cureus 2021, 13, e17345. [Google Scholar] [CrossRef]
  11. de Almeida, J.N.; Moreno, L.; Francisco, E.C.; Marques, G.N.; Mendes, A.V.; Barberino, M.G.; Colombo, A.L. Trichosporon asahii superinfections in critically ill COVID-19 patients overexposed to antimicrobials and corticosteroids. Mycoses 2021, 64, 817–822. [Google Scholar] [CrossRef]
  12. Duarte-Oliveira, C.; Rodrigues, F.; Gonçalves, S.M.; Goldman, G.H.; Carvalho, A.; Cunha, C. The Cell Biology of the Trichosporon-Host Interaction. Front. Cell. Infect. Microbiol. 2017, 7, 118. [Google Scholar] [CrossRef]
  13. Lo, S.; Tseng, Y.; Chen, Y.; Ho, M.; Lee, C.; Lu, P.; Lin, S. In vitro activity of isavuconazole, ravuconazole, and comparison of the Sensititre Yeast One and CLSI broth microdilution methods against clinical isolates of Trichosporon species. J. Clin. Microbiol. 2025, 63, e00319-25. [Google Scholar] [CrossRef]
  14. Chen, S.C.; Perfect, J.; Colombo, A.L.; Cornely, O.A.; Groll, A.H.; Seidel, D.; Albus, K.; de Almedia, J.N., Jr.; Garcia-Effron, G.; Gilroy, N.; et al. Global guideline for the diagnosis and management of rare yeast infections: An initiative of the ECMM in cooperation with ISHAM and ASM. Lancet Infect. Dis. 2021, 21, e375–e386. [Google Scholar] [CrossRef] [PubMed]
  15. de Almeida Júnior, J.N.; Hennequin, C. Invasive Trichosporon Infection: A Systematic Review on a Re-emerging Fungal Pathogen. Front. Microbiol. 2016, 7, 1629. [Google Scholar] [CrossRef]
  16. Ellsworth, M.; Ostrosky-Zeichner, L. Isavuconazol: Mecanismo de ação, eficácia clínica e resistência. J. Fungi 2020, 6, 324. [Google Scholar] [CrossRef] [PubMed]
  17. Feugray, G.; Krzisch, D.; Dehais, M.; Razakandrainibe, R.; Gargala, G.; Favennec, L.; Leprêtre, S.; Camus, V.; Costa, D. Successful treatment of Trichosporon asahii fungemia with isavuconazole in a patient with hematologic malignancies. Infect. Drug Resist. 2019, 12, 2015–2018. [Google Scholar] [CrossRef]
  18. Itoh, K.; Iwasaki, H.; Negoro, E.; Shigemi, H.; Tokimatsu, I.; Tsutani, H.; Yamauchi, T. Successful treatment of breakthrough Trichosporon asahii fungemia by the combination therapy of fluconazole and liposomal amphotericin B in a patient with follicular lymphoma. Mycopathologia 2021, 186, 117–121. [Google Scholar] [CrossRef] [PubMed]
  19. Silvestre Junior, A.M.; Miranda, M.A.B.R.; Camargo, Z.P.D. Trichosporon species isolated from the perigenital region, urine and catheters of a Brazilian population. Braz. J. Microbiol. 2010, 41, 628–634. [Google Scholar] [CrossRef]
  20. Diogo, H.C.; Sarpieri, A.; Pires, M.C. Preservação de fungos em água destilada. An. Bras. Dermatol. 2005, 80, 591–594. [Google Scholar] [CrossRef]
  21. CLSI. Method for Antifungal Disk Diffusion Susceptibility Testing of Yeasts, 3rd ed.; CLSI supplement M44; Clinical and Laboratory Standards Institute: Malvern, PA, USA, 2018. [Google Scholar]
  22. Pfaller, M.A.; Diekema, D.J.; Gibbs, D.L.; Newell, V.A.; Ellis, D.; Tullio, V.; Rodloff, A.; Fu, W.; Ling, T.A.; Global Antifungal Surveillance Group. Results from the ARTEMIS DISK Global Antifungal Surveillance Study, 1997 to 2007: A 10.5-year analysis of susceptibilities of Candida Species to fluconazole and voriconazole as determined by CLSI standardized disk diffusion. J. Clin. Microbiol. 2010, 48, 1366–1377. [Google Scholar] [CrossRef]
  23. Menezes, E.A.; Marinho, J.A.; Angelo, M.R.; Cunha, M.d.C.; Cunha, F.A.; Vasconcelos Júnior, A.A. Isolation and antifungal susceptibility testing of Trichosporon asahii in Ceará, Brazil. Rev. Inst. Med. Trop. Sao Paulo 2012, 54, 1–3. [Google Scholar] [CrossRef] [PubMed]
  24. Liofilchem. Discs for Antigungal Susceptibility Test of Yeasts; Antifungal Disc. Terano, Liofilchem: Roseto degli Abruzzi, Italy, 2021. [Google Scholar]
  25. CLSI. Performance Standards for Antifungal Susceptibility Testing of Yeasts, 2nd ed.; CLSI supplement M60; Clinical and Laboratory Standards Institute: Wayne, PA, USA, 2020. [Google Scholar]
  26. Li, H.; Guo, M.; Wang, C.; Li, Y.; Fernandez, A.M.; Ferraro, T.N.; Yang, R.; Chen, Y. Epidemiological study of Trichosporon asahii infections over the past 23 years. Epidemiol. Infect. 2020, 148, e169. [Google Scholar] [CrossRef]
  27. Alboloshi, G.J.; Jiman-Fatani, A.; Attallah, D.; Mokhtar, J.; Al-Abdullah, N.A.; Alkuwaity, K.; Kaki, R.; Al-Rabia, M.W.; Alfadil, A.; Ibrahem, K.; et al. The Prevalence and Risk Factors of Trichosporonosis at King Abdulaziz University Hospital. Int. J. Gen. Med. 2024, 17, 1297–1310. [Google Scholar] [CrossRef]
  28. Martínez-Herrera, E.; Duarte-Escalante, E.; Reyes-Montes, M.D.R.; Arenas, R.; Acosta-Altamirano, G.; Moreno-Coutiño, G.; Vite-Garín, T.M.; Meza-Robles, A.; Frías-De-León, M.G. Molecular identification of yeasts from the order Trichosporonales causing superficial infections. Rev. Iberoam. Micol. 2021, 38, 119–124. [Google Scholar] [CrossRef]
  29. Andrade, I.B.; de Sousa Araújo, G.R.; Brito-Santos, F.; Figueiredo-Carvalho, M.H.G.; Zancopé-Oliveira, R.M.; Frases, S.; Almeida-Paes, R. Comparative biophysical and ultrastructural analysis of melanins produced by clinical strains of different species from the Trichosporonaceae family. Front. Microbiol. 2022, 13, 876611. [Google Scholar] [CrossRef]
  30. Montoya, A.M.; González, A.S.; Palma-Nicolás, J.P.; Gómez-Treviño, A.; González, J.G.; González, G.M. Genotyping, extracellular compounds, and antifungal susceptibility testing of Trichosporon asahii isolated from Mexican patients. Med. Mycol. 2015, 53, 505–511. [Google Scholar] [CrossRef] [PubMed]
  31. Robles-Tenorio, A.; Lepe-Moreno, K.Y.; Mayorga-Rodríguez, J. White Piedra, a Rare Superficial Mycosis: An Update. Curr. Fungal Infect. Rep. 2020, 14, 197–202. [Google Scholar] [CrossRef]
  32. Lopez Luis, B.A.; León-Palacios, K.A.; Acosta-Ruiz, A.; Gonzalez-Cardel, A.M.; Rodriguez-Zuñiga, G. Clinical significance of nosocomial Trichosporon asahii in urine: A retrospective cohort study. Infect. Dis. Now 2025, 55, 105059. [Google Scholar] [CrossRef]
  33. Mattede, M.G.S.; Piras, C.; Mattede, K.D.S.; Ferrari, A.T.; Baldotto, L.S.; Assbu, M.S.Z. Infecções urinárias causadas por Trichosporon spp. em pacientes graves internados em unidade de terapia intensiva. Rev. Bras. Ter. Intensiv. 2015, 27, 247–251. [Google Scholar]
  34. Acampora, N.; Frizza, A.; Brau, F.; Torelli, R.; Vella, A.; De Carolis, E.; Fantoni, M. A case of Trichosporon asahii urinary tract infection in a frail elderly patient. Infez. Med. 2019, 27, 93–96. [Google Scholar] [PubMed]
  35. Cronyn, V.; Howard, J.; Chiang, L.; Le, L.; Tims-Cook, Z.; Gertz, A.M. Trichosporon asahii Urinary Tract Infection in a Patient with Severe COVID-19. Case Rep. Infect. Dis. 2021, 2021, 6841393. [Google Scholar] [CrossRef]
  36. Turunen, J.; Paalanne, N.; Reunanen, J.; Tapiainen, T.; Tejesvi, M.V. Development of gut mycobiome in infants and young children: A prospective cohort study. Pediatr. Res. 2023, 94, 486–494. [Google Scholar] [CrossRef]
  37. Abegg, P.T.G.M.; Silva, L.L. Controle de infecção hospitalar em unidade de terapia intensiva: Estudo retrospectivo. Semin. Ciências Biológicas Saúde 2011, 32, 47–58. [Google Scholar] [CrossRef]
  38. Oliveira, A.C.; Paula, A.O.; Iquipaza, R.A.; Lacerda, A.C.S. Infecções relacionadas à assistência em saúde e gravidade clínica em uma unidade de terapia intensiva. Rev. Gaúcha Enferm. 2012, 33, 89–96. [Google Scholar] [CrossRef]
  39. Cordeiro, A.L.A.O.; Oliveira, M.M.C.; Fernandes, J.D.; Barros, C.S.M.A.; Castro, L.M.C. Equipment contamination in an intensive care unit. Acta Paul. Enferm. 2015, 28, 160–165. [Google Scholar] [CrossRef]
  40. Mahl, S.; Rossi, E.M. Susceptibilidade antimicrobiana de bactérias isoladas de colchões hospitalares. Rev. Bras. Análises Clínicas 2017, 49, 371–375. [Google Scholar]
  41. Mariné, M.; Brown, N.A.; Riaño-Pachón, D.M.; Goldman, G.H. On and Under the Skin: Emerging Basidiomycetous Yeast Infections Caused by Trichosporon Species. PLoS Pathog. 2015, 11, e1004982. [Google Scholar] [CrossRef]
  42. Ramírez, I.; Moncada, D. Fatal Disseminated Infection by Trichosporon asahii Under Voriconazole Therapy in a Patient with Acute Myeloid Leukemia: A Review of Breakthrough Infections by Trichosporon spp. Mycopathologia 2019, 185, 377–388. [Google Scholar] [CrossRef]
  43. Alonso, V.P.P.; Lemos, J.G.; Nascimento, M.D.S.D. Yeast biofilms on abiotic surfaces: Adhesion factors and control methods. Int. J. Food Microbiol. 2023, 400, 110265. [Google Scholar] [CrossRef]
  44. Piecuch, A.; Cal, M.; Ogórek, R. Adhesion and biofilm formation by two clinical isolates of Trichosporon cutaneum in various environmental conditions. Braz. J. Microbiol. 2024, 55, 1793–1800. [Google Scholar] [CrossRef]
  45. Ministério da saúde Triscosporonose. Available online: https://www.gov.br/saude/pt-br/assuntos/saude-de-a-a-z/t/triscosporonose (accessed on 3 February 2026).
  46. Yasir, M.; Goyal, A.; Sonthalia, S. Corticosteroid Adverse Effects; StatPearls Publishing: Treasure Island, FL, USA, 2025. Available online: https://www.ncbi.nlm.nih.gov/books/NBK531462/ (accessed on 3 February 2026).
  47. Bhatia, M. Trichosporon Infections: Background, Pathophysiology, Epidemiology. Medscape e Medicine. Atualizado em 30 Set. 2024. Available online: https://emedicine.medscape.com/article/230705-overview?form=fpf (accessed on 3 February 2026).
  48. de Sá, I.W.A.; Magalhães, M.D.A.; de Andrande, M.G.P.; de Araújo, S.G.L.; Domingues, M.T.D.S.; de Araújo, P.S.R.; Avelino, L.N.T.; Júnior, M.L.F. Infeccção de corrente sanguínea por Trichosporon asahii em paciente COVID-19. Braz. J. Infect. Dis. 2022, 26, 101801. [Google Scholar] [CrossRef]
  49. Gil, Ó.; Hernández-Pabón, J.C.; Tabares, B.; Lugo-Sánchez, C.; Firacative, C. Rare Yeasts in Latin America: Uncommon Yet Meaningful. J. Fungi 2023, 9, 747. [Google Scholar] [CrossRef]
  50. Nivoix, Y.; Ledoux, M.-P.; Herbrecht, R. Antifungal therapy: New and evolving therapies. Semin. Respir. Crit. Care Med. 2020, 41, 158–174. [Google Scholar] [CrossRef]
  51. Santos, C.O.; Zijlstra, J.G.; Porte, R.J.; Kampinga, G.A.; van Diepeningen, A.D.; Sinha, B.; Bathoorn, E. Emerging pan-resistance in Trichosporon species: A case report. BMC Infect. Dis. 2016, 16, 148. [Google Scholar] [CrossRef]
  52. Sprute, R.; Bethe, U.; Chen, S.C.-A.; Cornely, O.A. EQUAL Trichosporon Score 2022: An ECMM score to measure Quality of the clinical management of invasive Trichosporon infections. J. Antimicrob. Chemother. 2022, 77, 1779–1784. [Google Scholar] [CrossRef] [PubMed]
  53. Prasad, R.; Shah, A.H.; Rawal, M.K. Antifungals: Mechanism of action and drug resistance. Adv. Exp. Med. Biol. 2016, 892, 327–349. [Google Scholar]
  54. Basu, S.; Tilak, R.; Kumar, A. Multidrug-resistant Trichosporon: An unusual fungal sepsis in preterm neonates. Pathog. Glob. Health 2015, 109, 202–206. [Google Scholar] [PubMed]
  55. Lima, Y.P.; Dias, V.C. Trichosporon spp.: What’s new? Future Microbiol. 2024, 19, 373–375. [Google Scholar] [CrossRef] [PubMed]
  56. de Almeida, J.N.; Francisco, E.C.; Ruiz, A.H.; Cuéllar, L.E.; Aquino, V.R.; Mendes, A.V.; Queiroz-Telles, F.; Santos, D.W.; Guimarães, T.; Chaves, G.M.; et al. Epidemiology, clinical aspects, outcomes and prognostic factors associated with Trichosporon fungaemia: Results of an international multicentre study carried out at 23 medical centres. J. Antimicrob. Chemother. 2021, 76, 1907–1915. [Google Scholar] [CrossRef]
  57. World Health Organization. WHO Fungal Priority Pathogens List to Guide Research, Development and Public Health Action; WHO: Genebra, Switzerland, 2022; Available online: https://www.who.int/publications/i/item/9789240060241 (accessed on 3 August 2025).
  58. Brandt, M.E.; Park, B.J. Think fungus–prevention and control of fungal infections. Emerg. Infect. Dis. 2013, 19, 1688–1689. [Google Scholar] [CrossRef] [PubMed]
Figure 1. Macroscopic and microscopic features, respectively, were observed in isolates of species from the Trichosporonaceae family. Legend: (A) Macromorphology of Trichosporon spp. colonies on Sabouraud dextrose agar, showing dry, cerebriform colonies with white to cream coloration. (B) Micromorphology of Gram-stained Trichosporon spp., revealing pseudohyphae and arthroconidia. (C) Micromorphology of Trichosporon spp. stained with cotton blue, showing arthroconidia.
Figure 1. Macroscopic and microscopic features, respectively, were observed in isolates of species from the Trichosporonaceae family. Legend: (A) Macromorphology of Trichosporon spp. colonies on Sabouraud dextrose agar, showing dry, cerebriform colonies with white to cream coloration. (B) Micromorphology of Gram-stained Trichosporon spp., revealing pseudohyphae and arthroconidia. (C) Micromorphology of Trichosporon spp. stained with cotton blue, showing arthroconidia.
Jof 12 00167 g001
Figure 2. Distribution of Trichosporon and Cutaneotrichosporon species with corresponding clinical data. Legend: Icons represent sex (♂ male, ♀ female), hospitalization setting (Jof 12 00167 i001 hospitalized or Jof 12 00167 i002 non-hospitalized), and clinical condition (Jof 12 00167 i003 neonates, Jof 12 00167 i004 adults, and Jof 12 00167 i005 elderly (individuals older than 60 years)). The values indicate the absolute number and percentage of cases for each variable.
Figure 2. Distribution of Trichosporon and Cutaneotrichosporon species with corresponding clinical data. Legend: Icons represent sex (♂ male, ♀ female), hospitalization setting (Jof 12 00167 i001 hospitalized or Jof 12 00167 i002 non-hospitalized), and clinical condition (Jof 12 00167 i003 neonates, Jof 12 00167 i004 adults, and Jof 12 00167 i005 elderly (individuals older than 60 years)). The values indicate the absolute number and percentage of cases for each variable.
Jof 12 00167 g002
Figure 3. Sites of Trichosporonaceae isolation and frequency of invasive medical device use. Legend: (A) Anatomical distribution of clinical specimens from which Trichosporonaceae isolates were obtained (n = 40). (B) Distribution and frequency of use of invasive medical devices among individuals with Trichosporonaceae species (n = 33).
Figure 3. Sites of Trichosporonaceae isolation and frequency of invasive medical device use. Legend: (A) Anatomical distribution of clinical specimens from which Trichosporonaceae isolates were obtained (n = 40). (B) Distribution and frequency of use of invasive medical devices among individuals with Trichosporonaceae species (n = 33).
Jof 12 00167 g003
Table 1. Clinical and epidemiological characteristics of individuals with Trichosporonaceae infections.
Table 1. Clinical and epidemiological characteristics of individuals with Trichosporonaceae infections.
Clinical and Epidemiological ParametersTrichosporonaceae (n = 40)
Type of infection: n = 40
  Surface5 (12.5)
  Invasive35 (87.5)
Length of hospital stay (in days): average (range)34.8 (1–102)
Origin non-hospitalized: n = 40
        Non-hospitalized
    Origin hospitalized: n = 33
7 (17.5)
  Coronary unit1 (3.1)
  Impatient unit9 (27.2)
  Surgical center6 (18.1)
  General ICU4 (12.2)
  Neurological ICU11 (33.3)
         Neonatal ICU
    Reason for hospitalization: n = 33
2 (6.1)
  Cancer3 (9.1)
  Hemorrhage1 (3.1)
  Hydrocele and spermatocele1 (3.1)
  Respiratory infection8 (24.2)
  Heart failure1 (3.1)
  Liver failure1 (3.1)
  Acute renal failure7 (21.2)
  Respiratory failure2 (6.1)
  Osteomyelitis1 (3.1)
  Septicemia4 (12.2)
  Pulmonary tuberculosis1 (3.1)
  Pressure ulcer3 (9.1)
Clinical outcome: n = 33
  Hospital discharge16 (48.5)
  Death17 (51.5)
Prior use of corticosteroids: n = 33
  No12 (36.4)
  Yes21 (63.6)
Clinical condition: n = 40
  No25 (62.5)
  Yes15 (37.5)
    Yes—Hemodialysis4 (10.0)
    Yes—Prematurity/twins1 (2.5)
    Yes—Surgery1 (2.5)
    Yes—Transplant2 (5.0)
    Yes—Bronchoscopy6 (15.0)
    Yes—Bronchofibroscopy and video laparoscopy1 (2.5)
Table 2. Prescription of antimicrobial drugs before and after the diagnosis of fungal infection in all individuals, according to electronic medical records.
Table 2. Prescription of antimicrobial drugs before and after the diagnosis of fungal infection in all individuals, according to electronic medical records.
Clinical and Epidemiological ParametersTrichosporonaceae (n = 40)
Prior use of antimicrobials: 40n (%)
   No11 (27.5)
   Yes29 (72.5)
    Yes—Combination therapy24 (60.0)
    Yes—Ceftriaxone1 (2.5)
    Yes—Cefuroxime1 (2.5)
    Yes—Piperacillin-tazobactam3 (7.5)
Use of antifungals after diagnosis: 33
   No26 (65.0)
   Yes14 (35.0)
    Yes—Combination therapy3 (7.5)
    Yes—Fluconazole7 (17.5)
    Yes—Itraconazole3 (7.5)
    Yes—Nystatin1 (2.5)
Table 3. Factors associated with mortality in individuals with Trichosporonaceae infection (n = 33).
Table 3. Factors associated with mortality in individuals with Trichosporonaceae infection (n = 33).
VariableSurvivors
n (%)
Death
n (%)
OR
(95% CI)
p-Value
ICU admission3 (18.7)15 (88.2)32.5
(4.3–245.0)
<0.001
Prior use of antimicrobials11 (68.7)17 (100)16.3
(0.8–331.0)
0.018
Prior use of corticosteroids6 (37.5)15 (88.2)11.5
(2.0–66.0)
0.004
Use of antifungals after diagnosis4 (25.0)10 (58.8)4.3
(0.9–20.0)
0.080
Age *Lower medianHigher median0.004
Length of hospital stay *Shorter medianLonger median0.040
Legend: Data is presented as number (percentage) unless otherwise specified. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using bivariate analysis. Categorical variables were compared using Fisher’s exact test. Continuous variables (*) were compared using the Mann–Whitney U test. A p-value < 0.05 was considered statistically significant.
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Lima, Y.P.; Bastos, R.V.; de Andrade Bastos, V.Q.; de Andrade Bastos, L.Q.; Hipólito, J.R.; Bastos, A.N.; Diniz, C.G.; Da Silva, V.L.; Dias, V.C. Trichosporonaceae as (Re-)Emerging Pathogens: A Warning to the Medical Community. J. Fungi 2026, 12, 167. https://doi.org/10.3390/jof12030167

AMA Style

Lima YP, Bastos RV, de Andrade Bastos VQ, de Andrade Bastos LQ, Hipólito JR, Bastos AN, Diniz CG, Da Silva VL, Dias VC. Trichosporonaceae as (Re-)Emerging Pathogens: A Warning to the Medical Community. Journal of Fungi. 2026; 12(3):167. https://doi.org/10.3390/jof12030167

Chicago/Turabian Style

Lima, Yasmim Passos, Ricardo Villela Bastos, Victor Quinet de Andrade Bastos, Lucas Quinet de Andrade Bastos, João Renato Hipólito, André Netto Bastos, Cláudio Galuppo Diniz, Vania Lucia Da Silva, and Vanessa Cordeiro Dias. 2026. "Trichosporonaceae as (Re-)Emerging Pathogens: A Warning to the Medical Community" Journal of Fungi 12, no. 3: 167. https://doi.org/10.3390/jof12030167

APA Style

Lima, Y. P., Bastos, R. V., de Andrade Bastos, V. Q., de Andrade Bastos, L. Q., Hipólito, J. R., Bastos, A. N., Diniz, C. G., Da Silva, V. L., & Dias, V. C. (2026). Trichosporonaceae as (Re-)Emerging Pathogens: A Warning to the Medical Community. Journal of Fungi, 12(3), 167. https://doi.org/10.3390/jof12030167

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop