Clinically Important Emerging and Uncommon Fungal Pathogens in Asia: Epidemiology, Antifungal Resistance and Challenges in Diagnosis and Management

ABSTRACT

Fungal infections in Asia are influenced by warm, humid climates, high population density and expanding healthcare systems, which together facilitate the emergence, transmission and detection of both common and rare pathogens. While Candida and Aspergillus species remain the leading causes of invasive fungal disease, increasing attention has focused on uncommon yeasts and rare moulds, many of which show intrinsic or acquired antifungal resistance. Advances in molecular diagnostics and susceptibility testing have improved identification of emerging pathogens, including uncommon Candida species and rare moulds such as Mucorales, filamentous Basidiomycetes, non‐marneffei Talaromyces, Oomycetes and thermally dimorphic fungi like Emergomyces. These organisms primarily affect immunocompromised individuals and present significant diagnostic and therapeutic challenges due to identification difficulties, variable susceptibility patterns and limited clinical experience. Clinical presentations range from fungaemia and invasive pulmonary disease to cutaneous and disseminated infections. Treatment is guided by pathogen and susceptibility profiles, commonly involving echinocandins, amphotericin B and azoles. In some cases, particularly infections caused by Oomycetes and Mucorales, prompt surgical intervention is essential. This review provides a comprehensive overview of current epidemiological trends, risk factors, clinical features, antifungal susceptibility patterns and treatment outcomes associated with rare and emerging fungal pathogens in Asia. By highlighting these increasingly recognized infections, it aims to enhance awareness among clinicians and mycologists, promote evidence‐based diagnostic and therapeutic approaches and inform future research addressing this evolving and clinically significant public health challenge.

1. Introduction

Fungal infections in Asia are strongly shaped by environmental and ecological factors. Warm, humid climates across the region promote fungal growth and spore dispersal, while rapid urbanization and high population density increase exposure to airborne fungi and facilitate the spread of antifungal‐resistant species [1, 2, 3, 4]. These conditions contribute to the high prevalence and diversity of fungal diseases. The epidemiology varies: South Asia faces a high disease burden due to tropical climates, a high burden of patients in public sector hospitals and healthcare gaps; East Asia is seeing rising cases linked to urbanization and more immunocompromised individuals; and Southeast Asia's biodiversity and seasonal climate shifts allow a wide range of fungal pathogens to emerge, including regionally endemic species such as Talaromyces marneffei and uncommon yeasts and moulds [5, 6, 7, 8, 9].

While Candida and Aspergillus remain the most common causes of invasive fungal disease, reports of rare yeasts and moulds as aetiologic agents are steadily increasing, particularly among immunocompromised hosts [10, 11]. Advances in molecular identification (e.g., genomic sequencing, matrix‐assisted laser desorption/ionization time‐of‐flight mass spectrometry [MALDI‐TOF MS], PCR) and wider use of fungal susceptibility testing have revealed the clinical importance of uncommon yeasts such as Candida kefyr, Pichia (Candida) norvegensis and Candidozyma (Candida) auris, many of which show intrinsic or acquired antifungal resistance [12, 13, 14]. Likewise, rare moulds, including newly emerged species of Mucorales, filamentous Basidiomycetes, non‐marneffei species of Talaromyces and other unusual filamentous fungi, are being recognized with growing frequency, causing infections particularly in immunocompromised populations [15, 16, 17]. The emergence of these rare fungal pathogens presents significant diagnostic and therapeutic challenges, as emphasized in recent global and regional guidelines for non‐Aspergillus moulds [10, 11]. Limited clinical experience, variable antifungal susceptibility patterns and the lack of standardized treatment guidelines complicate patient management [18, 19]. For clinicians and mycologists across Asia, these infections represent a growing concern that requires greater recognition, improved diagnostics and further study.

This review summarizes the current knowledge of emerging and uncommon yeasts and moulds of clinical importance emerging in Asia. We highlight epidemiological trends, documented risk factors, clinical manifestations, diagnostic methods, antifungal susceptibility profiles where available and reported treatment outcomes, with the aim of supporting clinicians and researchers in addressing this evolving threat.

2. Materials and Methods

2.1. Literature Search Strategy

A systematic literature search was performed in PubMed to identify reports of emerging and uncommon fungal pathogens in Asia. The search was restricted to articles published in English between 1 January 2020 and 31 December 2025. Eligible publication types included case reports, case series, narrative reviews, systematic reviews, meta‐analyses and relevant books or guideline documents. The search strategy incorporated combinations of the following terms: “emerging fungal infections,” “neglected fungal pathogens,” “rare yeast infections,” “uncommon yeast infections,” “emerging yeast infections,” “non‐ Candida albicans ,” “rare molds,” “uncommon mold infections,” “filamentous fungal infections,” “opportunistic fungal infections,” “Basidiomycetes infections,” “fungal‐like,” “Oomycetes infections” and “oomycoses.” The reference lists of eligible articles were also manually reviewed to identify additional relevant publications. Duplicate records were removed before screening.

2.2. Study Screening and Pathogen Selection

After initial screening, duplicate articles and studies unrelated to human fungal infections in Asia were excluded. For the purpose of this review, ‘emerging’ fungal pathogens were defined as organisms demonstrating increasing recognition in clinical practice, expanding geographic distribution, newly recognized pathogenicity or evolving diagnostic and antifungal resistance challenges, rather than solely representing newly discovered species [20]. The remaining articles were reviewed to identify fungal pathogens that fulfilled the predefined pathogen selection criteria. Pathogens were eligible for inclusion if they were yeasts, moulds or fungal‐like organisms causing proven or probable human infection, were reported predominantly from Asian countries or demonstrated increasing recognition in Asia during the study period (2020–2025), and fulfilled at least one of the following criteria: (i) association with unusual clinical syndromes, novel host populations, outbreaks or high mortality; (ii) diagnostic challenges requiring advanced phenotypic or molecular identification methods beyond conventional microbiological techniques; or (iii) intrinsic or emerging antifungal resistance with potential therapeutic implications. To maintain the review's focus on under‐recognized pathogens, well‐established fungal pathogens with extensive clinical evidence and dedicated international guidelines, including common species of Candida and Aspergillus, as well as members of the order Mucorales, were excluded. Organisms with insufficient evidence supporting pathogenicity in humans were also excluded. In addition, pathogens with inadequate published data regarding clinical manifestations, antifungal susceptibility, treatment or outcomes were not considered suitable for detailed review. The study selection process is summarized in Figure 1. Using these predefined criteria, 27 fungal species representing 29 clinically relevant taxa were selected from 32 eligible publications for detailed review (Figure 1).

FIGURE 1.

Flow chart of literature screening and selection process.

2.3. Data Extraction and Synthesis

For each selected pathogen, available data regarding epidemiology, geographic distribution, host characteristics, clinical manifestations, diagnostic methods, antifungal susceptibility patterns, treatment approaches and clinical outcomes were extracted and summarized. Information from additional relevant publications identified through reference screening was incorporated when appropriate to provide broader clinical context and ensure comprehensive coverage. The extracted data were synthesized narratively, with emphasis on the epidemiology of these pathogens in Asia, emerging trends, diagnostic challenges, antifungal resistance and implications for clinical management.

3. Results and Discussions

In this review, we identified and summarized clinically significant emerging and uncommon yeasts and moulds in Asia, including Candidozyma (Candida) auris, Candidozyma (Candida) vulturna, Kluyveromyces marxianus, Pichia norvegensis, Candida khanbhai, Lodderomyces elongisporus, Apiotrichum mycotoxinivorans, Trichophyton indotineae, newly emerging Mucorales species, non‐marneffei Talaromyces species, filamentous basidiomycetes and Emergomyces species.

3.1. Rare Yeasts

3.1.1. Candidozyma (Candida) auris

Candidozyma auris was first identified in 2009 from the ear canal of a patient in Japan, hence the name ‘auris’, derived from the Latin word for ‘ear’ [21]. Whole‐genome sequencing of clinical C. auris strains has revealed six geographically distinct clades with differing virulence profiles [22, 23, 24]. Four of these clades originated in Asian countries (Bangladesh, India, Iran, Japan, Pakistan and Singapore) [23, 24]. However, the geographic attribution of individual clades should be interpreted cautiously because it is based largely on the locations where isolates were first recognized. Subsequent international transmission may obscure the true origins and current distribution of these clades. Importantly, C. auris exhibits clade‐dependent antifungal susceptibility [23, 24]. Clade II (East Asian) is typically susceptible to all major antifungal classes and predominantly causes ear infections, whereas Clades I, III and IV are frequently multidrug‐resistant, particularly in nosocomial outbreaks [23, 24]. Unlike other Candida species, C. auris preferentially colonizes human skin and non‐living surfaces, including medical devices, rather than the gastrointestinal tract [25, 26]. Microbiologically, it is a budding yeast closely related to C. haemulonii and C. duobushaemulonii [27]. Unlike C. albicans , C. auris rarely forms pseudohyphae in general conditions [28]. It cannot be reliably distinguished from other Candida species by conventional methods. However, it grows well at elevated temperatures (40°C–42°C) [21], produces smooth, white‐to‐cream‐coloured colonies [21], and the development of a new chromogenic medium (CHROMagar Candida Plus) enables rapid identification and differentiation from other species [29]. A recent discovery of a C. auris ‐specific adhesin, surface colonization factor 1 (Scf1), has highlighted its role in biofilm formation, long‐term colonization of skin and medical devices and virulence during invasive infection [30]. Interestingly, isolates from certain clades show increased susceptibility to UV‐C light, suggesting new possibilities for disinfection strategies in healthcare environments [31]. The most common mechanism of azole resistance in C. auris involves mutations in the ERG11 gene, which encodes the drug target lanosterol 14α‐demethylase [32, 33, 34]. Echinocandins are recommended as empirical or initial therapy, with micafungin preferred over caspofungin due to its lower minimum inhibitory concentrations (MICs) [35, 36]. Although resistance to echinocandins remains uncommon (around 5%), it may develop during treatment and is typically associated with FKS1 mutations [32, 33, 34]. Routine combination therapy is not currently recommended but may be considered on a case‐by‐case basis [37]. For example, liposomal amphotericin B combined with echinocandins has shown a synergistic effect, reducing the MIC of micafungin by up to 64‐fold in 8 of 10 isolates [38]. Additionally, in vitro studies indicate that combining posaconazole with protease inhibitors such as atazanavir or saquinavir enhances fungistatic activity and significantly reduces C. auris biofilm formation [39]. These findings are hypothesis‐generating but should be interpreted cautiously, as in vitro synergy does not necessarily translate into improved clinical outcomes. The small numbers of isolates studied, variation in synergy‐testing methods, potential toxicity, drug interactions and lack of controlled clinical data currently limit the applicability of these combinations in routine practice. Well‐designed multicentre clinical studies, supported by standardized susceptibility testing and genomic surveillance, are needed to define optimal treatment strategies.

3.1.2. Candidozyma (Candida) vulturna

Candidozyma vulturna, a recently recognized member of the C. haemulonii complex and closely related to C. auris , has emerged as an opportunistic human pathogen in Asia [40, 41, 42]. It was first isolated from flowers in Mindanao, the Philippines, in 2016 [43] and subsequently reported to cause bloodstream infections [44, 45]. Conventional identification methods, including VITEK2 and MALDI‐TOF, often misidentify C. vulturna as C. haemulonii, complicating accurate diagnosis [41, 42]. The species exhibits intrinsic resistance to azoles, with additional resistance observed to amphotericin B, fluconazole and voriconazole, while remaining susceptible to echinocandins such as anidulafungin and caspofungin [41, 42]. A recent narrative review [41] documented 94 cases over the past decade, including 3 clonal outbreaks in Brazil, Vietnam and China, with subsequent spread across multiple continents. Infections mainly affect males from Asia and Latin America, with typical risk factors for candidaemia, with an overall mortality of 18%. Phylogenetic analyses confirm C. vulturna's close relationship to C. auris and C. haemulonii, suggesting shared pathogenic traits [41]. Notably, C. vulturna demonstrates significant biofilm formation capabilities, relatively more than those in C. auris and C. haemulonii, contributing to its persistence in clinical environments [42]. In Malaysia, among 19 reported cases, 47% originated from Sabah, with additional cases from Klang Valley, Sarawak and other states, highlighting its regional clinical significance and underscoring the importance of susceptibility‐guided antifungal therapy [46]. Whether C. vulturna represents a genuinely emerging pathogen or has historically been under‐recognized remains uncertain, as earlier cases were likely misidentified because of the limited discriminatory ability of conventional diagnostic methods. The current understanding of C. vulturna remains constrained by the rarity of reported cases, reliance on retrospective observational studies and the absence of prospective multicentre cohorts.

3.1.3. Kluyveromyces marxianus (Candida kefyr)

Candida kefyr, whose teleomorph is classified as Kluyveromyces marxianus [47], was first isolated in 1909 from kefir, a fermented milk beverage [48]. Although it remains a rare cause of human disease, recent reports suggest that it may be an emerging pathogen, particularly among immunocompromised patients [48]. Cases have been described in individuals with haematologic malignancies, including allogeneic haematopoietic stem cell transplant recipients, in whom infection typically occurs 14–300 days post‐transplantation despite antifungal prophylaxis, as well as in kidney transplant recipients who did not receive prophylaxis [48]. Candida kefyr is notable for its ability to form biofilms and its high propensity to cause infection through colonization [49]. Antifungal susceptibility testing shows that most isolates are sensitive to commonly tested agents, with favourable responses observed to both azoles and amphotericin B, although reports of resistance have also been documented [48]. Compared with candidaemia caused by other Candida species, C. kefyr infection is generally associated with better outcomes and a lower mortality rate [48]. However, these observations should be interpreted cautiously because published studies include relatively few patients, often lack appropriate comparator groups and are susceptible to selection and publication bias.

3.1.4. Pichia (Candida) norvegensis

Recently reclassified as Pichia norvegensis [50], Candida norvegensis was first described in 1954 after being isolated from the sputum of three asthmatic patients in Norway [51]. Although infections caused by this species are rare, several potential risk factors have been reported, including human immunodeficiency virus (HIV) infection, which is associated with invasive and oropharyngeal candidiasis, and malignancies such as hepatocellular carcinoma, which have also been linked to invasive disease [52, 53, 54]. In addition to invasive candidiasis, P. norvegensis peritonitis has been documented in a renal transplant patient undergoing peritoneal dialysis [55], highlighting its potential to cause opportunistic infections in immunocompromised hosts. Although P. norvegensis has only recently gained clinical recognition, a study published in 2010 analysing data from 1997 to 2007 demonstrated a 5‐ to 10‐fold increase in the rate of P. norvegensis isolation over the study period, suggesting an increasing clinical relevance of this uncommon yeast [56].

Antifungal susceptibility profiles vary across published studies. Overall, P. norvegensis is resistant to fluconazole and flucytosine [57, 58]. In contrast, susceptibility to voriconazole and echinocandins has been inconsistent, with variable results reported among different isolates and studies [58, 59]. Amphotericin B has traditionally been regarded as the treatment of choice [58, 60], despite limited supporting evidence from the small number of documented infections. More recently, several reports have demonstrated susceptibility of P. norvegensis isolates to echinocandins [56, 61, 62, 63], suggesting these agents as potential therapeutic alternatives.

3.1.5. Candida khanbhai

Named in honour of Prof. Dr. Ziauddin Khan (with ‘bhai’ meaning ‘friend’ or ‘brother’ in Hindi), it has only two reported clinical isolates to date [64]. The first was obtained from nasal colonization of a patient during a C. auris nosocomial outbreak in Kuwait in 2019, initially misidentified as C. duobushaemulonii by VITEK 2 (bioMérieux) with 99% probability [64]. The second was isolated in 2014 from the blood culture of a 55‐year‐old man with no known comorbidities, who had been hospitalized for the treatment of new‐onset hospital‐acquired pneumonia in Malaysia. This isolate was biochemically identified as Clavispora (Candida) lusitaniae by API 20C (bioMérieux) with 81% probability. Despite starting 400 mg/day of intravenous fluconazole on Day 12 of admission, the patient's condition deteriorated, and he died [64]. Subsequent sequence‐based analysis using the ITS1‐5.8S‐ITS2 region and the D1/D2 domain of the large subunit rDNA confirmed these isolates as a distinct lineage basal to the C. haemulonii species complex, which includes the clinically relevant species C. duobushaemulonii, C. pseudohaemulonii and C. vulturna [64]. Conventional laboratory methods often misidentify isolates, underscoring the need for advanced diagnostic approaches. Phenotypically, colonies were off‐white, glossy, soft and butyrous with entire margins. Cells were ovoid to spherical (1.5–3.5 × 2.5–4.5 μm), occurring singly, in pairs or short chains, with monopolar budding and no pseudohyphae observed after up to 12 weeks of incubation [64]. On chromogenic agar (Candida Plus), colonies appeared pale cream to lavender, with a distinctive blue halo like that of C. auris . MALDI‐TOF MS failed to yield a definitive match, with the closest hits to C. pseudohaemulonii and Clostridium cadaveris [64]. Biochemically, isolates exhibited delayed but positive maltose fermentation, no growth in 50%–60% glucose, tolerance to 0.1% cycloheximide and growth at up to 42°C [64]. Antifungal susceptibility testing revealed high MICs to amphotericin B and azoles, underscoring its potential clinical significance and diagnostic challenges [64]. However, these observations are based on only two isolates and should not be interpreted as representative of the species as a whole.

3.1.6. Lodderomyces elongisporus

First described as Saccharomyces elongisporus in 1952 [65], it is a homothallic fungus capable of sexual reproduction with multiple ascospore formation [66]. It has been isolated from soil, fermented food products, plants, stored apples, pigeon excreta, insects, marine fish and humans, and it can survive in hospital environments [67, 68, 69, 70, 71, 72], with reports of nosocomial infections, including an outbreak in a neonatal care unit [72]. To date, more than 40 human cases of L. elongisporus infection have been reported worldwide [73]. Most infections occur at the extremes of age, particularly in neonates and elderly patients [73]. Reported risk factors include malignancy (especially gastrointestinal cancers), while comorbid conditions such as heart disease, advanced malignancy and end‐stage renal disease have been associated with fatal outcomes in adults [73]. The most common clinical presentation is bloodstream infection, though invasive disease with oropharyngeal infections, endocarditis, osteomyelitis and meningitis [74, 75, 76] has also been documented. Its medical significance was first recognized in 2008 when a retrospective review of 542 clinical Candida parapsilosis isolates from 25 countries revealed that 10 were actually L. elongisporus [77]. This species closely resembles C. parapsilosis , displaying oval to elongated yeast cells or pseudohyphal forms, cream‐coloured colonies on Sabouraud dextrose agar and the ability to assimilate high‐molecular‐weight paraffins, which often leads to misidentification by conventional methods [77, 78]. ITS rDNA sequencing has been used to resolve such discrepancies, particularly when MALDI‐TOF identified L. elongisporus in isolates misclassified by RapID Yeast Plus as C. parapsilosis , C. stellatoidea or Geotrichum spp. [79]. Phylogenetic analyses show a slightly larger genome size (15–16 Mb) compared to C. parapsilosis (12–13 Mb), and it belongs to the CTG clade, where the CUG codon is translated as serine instead of leucine, along with other human pathogens such as C. albicans , C. tropicalis and C. lusitaniae [73, 80]. Distinguishing features include greater sensitivity to salinity, hydrogen peroxide and pH fluctuations, maintenance of the yeast form within phagocytes, and lower biofilm production (similar to C. parapsilosis ) than C. albicans, C. tropicalis and C. dubliniensis. However, reports of increased MICs to sodium hypochlorite and isolation from catheter tips suggest biofilm‐forming potential [81]. These characteristics indicate that L. elongisporus has various adaptive mechanisms that enable persistence and pathogenicity in clinical settings [81]. A 2023 case series reported antifungal susceptibility testing of L. elongisporus, demonstrating generally low MICs for most antifungal agents [82]. Notably, three patients received echinocandins to treat L. elongisporus fungaemia, with favourable outcomes [82]. These findings should be interpreted cautiously because treatment recommendations are based almost exclusively on observational data involving a small number of patients. No species‐specific clinical breakpoints or prospective therapeutic studies are available, and current management is largely extrapolated from guidelines for candidaemia caused by other Candida species.

3.1.7. Apiotrichum mycotoxinivorans

Apiotrichum mycotoxinivorans was first described in 2004 and is classified within the Basidiomycetes [83]. Formerly designated Trichosporon mycotoxinivorans, it was reclassified in 2015 based on updated phylogenetic analyses [84]. The organism has been isolated from environmental sources, including soil and river water, as well as from farm animals [85]. It was initially recognized as an emerging pathogen causing pulmonary infections, particularly among patients with cystic fibrosis, with the first clinical report published in 2009 [86]. Subsequently, an increasing number of extrapulmonary infections have been documented in Thailand, China, India, Latin America, the United States and several European countries [87, 88, 89, 90]. Reported clinical manifestations include fungaemia in patients with end‐stage renal disease receiving haemodialysis [87], intra‐abdominal abscesses following pancreaticoduodenectomy [87] and meningitis in a patient with B‐cell acute lymphoblastic leukaemia after neurosurgical intervention [88, 89]. Notably, two cases of haemodialysis‐associated bloodstream infection with concomitant Stenotrophomonas maltophilia bacteraemia have been described [87], although the clinical significance of this association remains unclear. Therefore, routine empirical antibacterial therapy cannot be recommended solely on the basis of the currently available evidence.

Morphologically, A. mycotoxinivorans produces oval to cuboid yeast‐like cells forming arthroconidia arranged in a characteristic beaded pattern, and colonies typically display a milky appearance [91]. For laboratory identification, MALDI‐TOF MS has emerged as a reliable and rapid alternative to PCR‐based methods for identifying rare fungal pathogens [88]. Antifungal susceptibility testing generally reveals low MICs for voriconazole but elevated MICs for amphotericin B [87, 88, 89]. Voriconazole is therefore considered the treatment of choice for invasive A. mycotoxinivorans infections [87, 88], and combination therapy with antibacterial agents may be appropriate, given the frequent occurrence of bacterial co‐infection [87]. However, correlations between in vitro susceptibility results and clinical outcomes remain poorly defined due to the limited number of reported invasive cases [88]. The overall reported mortality rate is approximately 50% [87]. However, according to limited reports, the mortality attributable specifically to A. mycotoxinivorans remains unclear and further studies are warranted.

Clinical characteristics, risk factors and antifungal susceptibility of rare yeasts were shown in Table 1.

TABLE 1.

Summary of species misidentification, initial diagnostic methods, risk factors, clinical manifestations, antifungal susceptibility patterns and preferred treatment options for emerging uncommon yeasts reported predominantly in Asia.

Species	Misidentification (initial diagnostic methods)	Risk factors	Clinical manifestations	Antifungal susceptibility patterns based on MIC testing	Preferred treatment options	References
Candidozyma (Candida) auris	Candida haemulonii (morphological identification, conventional biochemical test, commercial automated biochemical yeast identification systems, MALDI‐TOF MS) Candida duobushaemulonii (morphological identification, commercial automated biochemical yeast identification systems) Candida lusitaniae (commercial automated biochemical yeast identification systems, MALDI‐TOF MS)	Advanced age, prior skin colonization, recent surgery, indwelling devices, immunocompromised states (neutropenia, glucocorticoid use, organ transplant recipient)	Skin colonization (nares, axilla, groin), candidaemia, myopericarditis, meningitis, hepatosplenic infections, osteomyelitis, urinary tract infections, endophthalmitis, ear infections, wound infections	Clade‐dependent susceptibility: Azoles: mostly resistance Amphotericin B: variable Echinocandins: mostly susceptible	Echinocandins (especially micafungin), amphotericin B	[22, 23, 24, 92]
Candidozyma (Candida) vulturna	Candida haemulonii (commercial biochemical testing, commercial automated biochemical yeast identification systems, MALDI‐TOF MS) Candida duobushaemulonii (MALDI‐TOF MS) Candida pseudohaemulonii (MALDI‐TOF MS)	Male, immunocompromised states (neutropenia, endovascular catheters, haematologic malignancy)	Catheter‐related blood stream infection	MIC50 Fluconazole (n = 52): 32 μg/mL Voriconazole (n = 52): 0.25 μg/mL Amphotericin B (n = 44): 4 μg/mL Micafungin (n = 47): 0.06 μg/mL	Echinocandins, amphotericin B	[41, 93]
Kluyveromyces marxianus (Candida kefyr)	No report	Haematologic malignancies, solid organ (kidney) and haematologic stem cell transplant recipients	Candidaemia, catheter‐related blood stream infection, keratitis	Median MIC Fluconazole (n = 6): 0.25 μg/mL Voriconazole (n = 4): 0.012 μg/mL Amphotericin B (n = 4): 0.5 μg/mL Caspofungin (n = 2): 0.019 μg/mL	Fluconazole, amphotericin B, caspofungin, nystatin	[48]
Pichia (Candida) norvegensis	No report	HIV infection, malignancies, kidney transplant, peritoneal dialysis	Oropharyngeal candidiasis, peritonitis	MIC50 Fluconazole (n = 18): 32 μg/mL Itraconazole (n = 18): 0.25 μg/mL Voriconazole (n = 18): 0.5 μg/mL Amphotericin B (n = 18): 0.25 μg/mL Micafungin (n = 18): 0.064 μg/mL	Amphotericin B, echinocandins	[58]
Candida khanbai	Candida duobushaemulonii (commercial automated biochemical yeast identification systems) Candida pseudobushaemulonii (commercial biochemical testing, MALDI‐TOF MS) Clostridium cadaveris (MALDI‐TOF MS)	Hospital‐acquired pneumonia	Candidaemia	Median MIC Fluconazole (n = 2): > 48 μg/mL Itraconazole (n = 2): 12 μg/mL Voriconazole (n = 2): 9 μg/mL Amphotericin B (n = 2): 4 μg/mL Micafungin (n = 2): 0.3125 μg/mL	Echinocandins	[64]
Lodderomyces elongisporus	Candida parapsilosis, Candida stellatoidea, Geotrichum spp. (commercial biochemical testing)	Catheter‐related infections, neonatal ICU, nosocomial outbreaks	Fungaemia, endocarditis	Median MIC Fluconazole (n = 11): 0.25 μg/mL Voriconazole (n = 11): 0.015 μg/mL Amphotericin B (n = 10): 0.25 μg/mL Micafungin (n = 8): 0.032 μg/mL	Echinocandins	[79, 82]
Apiotrichum mycotoxinivorans	No report	Catheter‐related infections, post‐major surgery	Fungaemia, complicated intra‐abdominal infection, post‐neurosurgical meningitis	Median MIC Voriconazole (n = 2): 0.12 μg/mL Amphotericin B (n = 3): 2 μg/mL	Voriconazole	[87]

Abbreviations: HIV, human immunodeficiency virus; ICU, intensive care unit; MALDI‐TOF MS, Matrix‐Assisted Laser Desorption/Ionization Time‐of‐Flight Mass Spectrometry; MIC, minimum inhibitory concentration; n, number of isolates tested.

3.2. Rare Moulds

3.2.1. Emerging Species of Mucorales

The Mucorales order, a group of non‐septate hyphal fungi that includes Rhizopus, Rhizomucor, Mucor, Lichtheimia, Apophysomyces, Cunninghamella and Saksenaea, causes mucormycosis through angioinvasion [94]. The primary route of infection is inhalation of fungal conidia. Typically, mucormycosis presents as rhinocerebral disease in patients with uncontrolled diabetes mellitus and as pulmonary disease in immunocompromised individuals, particularly those with haematologic malignancies undergoing intensive chemotherapy or haematopoietic stem cell transplantation [95]. Among the Mucorales, Rhizopus spp., especially R. arrhizus, are the most common aetiologic agents of invasive disease. Rhizopus homothallicus, previously considered an environmental species, has emerged in over the past decade as a human pathogen, with an increasing number of cases reported in India [96, 97]. A retrospective study from India found that R. homothallicus accounted for 6.8% (43/631) of mucormycosis cases [98]. Molecular analysis using 18S rRNA gene sequencing and amplified fragment length polymorphism (AFLP) revealed distinct clustering of R. homothallicus, confirming its differentiation from other Rhizopus species [98]. Compared to R. arrhizus, R. homothallicus infections occurred in younger patients (mean age 45.9 vs. 52.5 years), exhibited slower‐growing colonies that were cottony white turning greyish to olive‐brown, with less prominent rhizoids and abundant golden zygospores [98]. The clinical manifestations of R. homothallicus were not different from those of R. arrhizus infection, except for a significantly higher frequency of visual disturbances (43.9% vs. 12.7%) [98]. Clinically, infections were also associated with a better survival rate (9.8% vs. 3.9%) [98]. Antifungal susceptibility testing demonstrated generally lower MICs for amphotericin B (0.03–16 μg/mL), itraconazole (0.03–16 μg/mL), posaconazole (0.03–8 μg/mL) and isavuconazole (0.03–16 μg/mL) compared to R. arrhizus [98]. In addition to Rhizopus species, several less common Mucorales have also been identified as human pathogens [99]. Apophysomyces variabilis, the second most commonly isolated species in India [99], is associated with necrotizing cutaneous infections in immunocompetent hosts following trauma [100], while Saksenaea vasiformis typically causes localized infections after contaminated injuries [101]. Mucor irregularis is linked to primary cutaneous disease in immunocompetent individuals [102], and Thamnostylum lucknowense has been reported as a rare cause of rhinocerebral mucormycosis in patients with poorly controlled diabetes mellitus [103]. Because conventional morphological identification may be unreliable for rare Mucorales, molecular methods are increasingly important for accurate species identification, epidemiological surveillance and understanding regional diversity.

3.2.2. Filamentous Basidiomycetes

The phylum Basidiomycota, which includes fungi commonly referred to as mushrooms, also contains well‐known human pathogenic yeast species such as Cryptococcus spp., Trichosporon spp. and Malassezia spp. Although filamentous basidiomycetes are rare causes of invasive fungal infections in humans, their clinical significance has become increasingly recognized, particularly in the context of chemotherapy, organ transplantation and novel immunosuppressive therapies [16]. Improved post‐transplant outcomes allow recipients to travel more often, increasing exposure to uncommon pathogens. The largest review in 2014 summarized 218 cases worldwide, with Schizophyllum commune being the most common species (n = 114; 52.3%) [16]. Schizophyllum commune is an edible, wood‐decaying fungus that causes respiratory infections, such as sinusitis and allergic bronchopulmonary mycosis (ABPM), and extra‐respiratory disease, including onychomycosis, brain abscess, meningitis and palate ulceration. Hormographiella aspergillata (n = 13; 5.9%), the anamorph of Coprinus cinereus found in compost and sewage, has been linked to invasive infections in patients with haematologic malignancies, including disseminated disease, endophthalmitis, infective endocarditis and pneumonia. Ceriporia lacerata (n = 11; 5%), a wood‐decaying fungus, was associated with pneumonia in chronic lung disease. A 2024 series described seven Volvariella volvacea infections (7/8 from Asia) in transplant or chemotherapy patients, presenting with pneumonia, brain lesions, skin lesions and infective endocarditis [104]. Other reported species include Inonotus tropicalis, Irpex lacteus, Phellinus undulatus, Perenniporia spp., Bjerkandera adusta, Sporotrichum pruinosum, Phanerochaete sordida and Cyclomyces tabacinus. Most cases occurred in Japan (n = 94; 43%) and India (n = 57; 26%), with the respiratory tract being the most affected site (n = 71), including 34 ABPM cases [16]. Colonies are typically cottony and white. Clamp connections, hyphal bridges that facilitate dikaryon formation, are infrequently observed in clinical isolates, which are generally monokaryotic (n); however, dikaryotization (2n) can be induced through mating with a compatible strain. Owing to the frequent absence of distinctive morphological features, phenotypic identification is often unreliable, rendering molecular identification essential. This is commonly achieved by sequencing the ribosomal ITS region and the D1/D2 domains of the large subunit (LSU) ribosomal DNA [16]. Antifungal susceptibility testing generally demonstrates low MICs for itraconazole, voriconazole, posaconazole and amphotericin B, whereas MICs for fluconazole and echinocandins are typically elevated. Clinical outcomes have been heterogeneous, and a standardized treatment regimen has yet to be established [16, 104]. Current management relies largely on extrapolation from case reports and expert opinion rather than high‐quality clinical evidence. Reported outcomes are highly heterogeneous and likely influenced by the infecting species, host immune status, disease extent and the feasibility of surgical intervention in addition to antifungal therapy.

3.2.3. Human Non‐marneffei Talaromyces

Talaromyces marneffei is a thermally dimorphic fungus endemic to southern China and the northern regions of Southeast Asia, including Thailand, with bamboo rats (Rhizomys spp.) serving as its natural reservoir [9, 105]. Infection occurs through inhalation of airborne conidia, most often causing systemic fungal disease in individuals with HIV infection [9]. Clinically, it frequently presents with generalized umbilicated papular skin lesions [9]. However, emerging data have identified new risk groups beyond HIV, including patients undergoing cancer treatment, organ transplant recipients and individuals receiving immunosuppressive therapy [9, 106]. Standard treatment includes amphotericin B followed by itraconazole [107]. Between 2006 and 2020 [108, 109, 110, 111, 112], several cases of human talaromycosis caused by non‐marneffei Talaromyces species have been reported worldwide, particularly in Asia. Reported species include T. amestolkiae [109], T. purpurogenus [108], T. piceus [110], T. subaurantiacus [111], T. kabodanensis [111], T. minnesotensis [111], T. rapidus [111], T. alveolaris [111] and T. atroroseus [112]. Reported risk factors include HIV infection, haematologic malignancies [108, 109] and chronic granulomatous disease [110]. Pulmonary involvement is the most common clinical manifestation. A notable study from Indonesia examined 10 clinical and environmental isolates of Talaromyces spp. recovered from patients and from rats captured in patients' homes [112]. Initially, all isolates were phenotypically identified as T. marneffei; however, subsequent molecular analysis revealed that nine of them were actually T. atroroseus [112]. These misidentified isolates differed morphologically from T. marneffei, lacking soluble red pigment production in agar and showing more filamentous growth, with longer and fragmented hyphae [112]. Antifungal susceptibility testing using Sensititre revealed that T. atroroseus exhibits high MICs for amphotericin B and echinocandins but low MICs for itraconazole and posaconazole [112]. As a result, treatment of non‐marneffei talaromycosis, particularly due to T. atroroseus, should be guided by antifungal susceptibility testing rather than standard protocols alone [112]. Overall, the available evidence indicates that non‐marneffei Talaromyces species represent an emerging but poorly characterized group of opportunistic pathogens. Current knowledge is constrained by the rarity of reported cases, publication bias, and reliance on retrospective case reports.

3.2.4. Emergomyces spp.

Emergomycosis is a systemic mycosis caused by thermally dimorphic fungi of the genus Emergomyces, previously classified within Emmonsia and belonging to the phylum Ascomycota [113]. Human infection is presumed to occur through inhalation of airborne conidia originating from soil, where these organisms persist as saprobes [114]. Among recognized species, Emergomyces africanus accounts for the majority of cases (71.4%), followed by E. pasteurianus, E. canadensis , E. crescens, E. orientalis and E. europaeus [114]. Although more than 70% of reported cases originate from South Africa [115, 116], emergomycosis is increasingly recognized in Asia and North America (each 9.1%). In Asia, infections are predominantly caused by E. pasteurianus and E. orientalis , with cases reported from China, Hong Kong and India [117, 118]. The disease primarily affects immunocompromised individuals, particularly those with advanced HIV infection (CD4 < 100 cells/μL) often accompanied by anaemia or thrombocytopenia, in this population, E. africanus is the most frequently implicated species [114]. In contrast, non‐HIV‐infected patients, including solid organ transplant recipients and those with diabetes mellitus or chronic kidney disease, are more commonly infected by non‐africanus species [114]. Clinical manifestations range from localized pulmonary disease to disseminated infection and fungaemia. Cutaneous involvement is prominent in HIV‐associated disease, with 75%–95% of patients presenting with polymorphic skin lesions such as papules, nodules, ulcers, verrucous plaques and crusted lesions, whereas non‐HIV patients more often present with predominant respiratory symptoms [114].

Definitive diagnosis relies on a combination of fungal culture and histopathological examination, although findings are frequently nonspecific and may mimic histoplasmosis or blastomycosis [119]. Histopathology typically demonstrates small intracellular yeasts with narrow‐based budding within granulomatous or suppurative dermal infiltrates [118]. Culture remains essential for species‐level identification. On Sabouraud dextrose agar, colonies are yellowish white to tan, initially glabrous, later becoming powdery and furrowed and typically reaching 2.5–3.5 cm in diameter within 3 weeks. At 24°C, the mould phase is characterized by slender conidiophores arising at right angles from hyphae and forming characteristic ‘floret’ structures composed of short secondary conidiophores bearing single, small, subspherical conidia [118]. At 37°C, the yeast phase consists of abundant ovoid yeast cells exhibiting unipolar narrow‐based budding with minimal hyphal elements, confirming thermal dimorphism [118]. Despite antifungal therapy, emergomycosis is associated with high mortality rates ranging from 31% to 46% [118]. Nevertheless, induction therapy with amphotericin B followed by oral itraconazole has been associated with improved clinical outcomes and survival [118]. Emergomycosis is an increasingly recognized opportunistic fungal infection whose epidemiology appears to vary substantially by geographic region, infecting species and host immune status. However, current understanding remains constrained by limited surveillance, diagnostic challenges and reliance on retrospective case reports and observational studies.

3.2.5. Trichophyton indotineae

Trichophyton indotineae, formerly designated T. mentagrophytes genotype VIII, is an emerging anthropophilic dermatophyte first described in India in 2020 [120]. It has since become a significant public health concern owing to its high transmissibility, which occurs predominantly through direct skin‐to‐skin contact. Indirect transmission has also been documented via contaminated fomites and environments, including bathrooms, clothing and bed linens [121]. Clinically, T. indotineae most commonly causes tinea corporis, tinea cruris and tinea genitalis, with a rising incidence of tinea faciei [120, 121, 122]. Infections caused by this species are typically more extensive and severe than those associated with other prevalent dermatophytes, such as T. rubrum and T. mentagrophytes [120, 121, 122]. The disease course is frequently chronic and relapsing, characterized by highly inflammatory, scaly, hyperpigmented and intensely pruritic lesions, most often involving the lower trunk and inguinal regions [120, 121, 122]. Since its initial identification, T. indotineae has been reported across Asia, the Middle East, Europe and the Americas, indicating rapid global dissemination [123]. Morphologically, it is indistinguishable from members of the T. mentagrophytes complex based on culture characteristics alone [123]. However, biochemical testing may aid preliminary differentiation, as T. indotineae is urease‐negative, in contrast to T. interdigitale and T. mentagrophytes, which are urease‐positive [123]. A major therapeutic challenge is the high prevalence of terbinafine resistance [121]. This resistance is mediated by multiple mechanisms, including efflux pump overexpression, biofilm formation and point mutations in the ERG1 gene encoding squalene epoxidase (SQLE), which reduce antifungal binding affinity [121].

Systemic itraconazole remains the treatment of choice. Standard dosing of 200 mg daily for 2 weeks, with extension up to 12 weeks in refractory cases, has demonstrated favourable outcomes, with no clear benefit observed from higher dosing regimens [121]. The super‐bioavailable (SUBA)‐itraconazole formulation, administered at 50 mg twice daily for 4 weeks, has also shown good clinical efficacy [121]. Adjunctive topical therapy with azoles, including clotrimazole, ketoconazole, luliconazole or bifonazole, may further improve treatment response when combined with systemic antifungal therapy [124]. Topical agents alone are generally insufficient for disease eradication but may serve a supportive role [121]. Although clinical experience remains limited, voriconazole has demonstrated promising in vitro activity and may be considered as salvage therapy in refractory infections [121]. In contrast, other systemic antifungal agents, including terbinafine, fluconazole, ketoconazole and griseofulvin, generally exhibit limited clinical efficacy against T. indotineae [121]. Trichophyton indotineae represents an important example of the intersection between antifungal resistance, inappropriate antifungal prescribing practices, and global dissemination. While evidence supporting its emergence and resistance is compelling, current management strategies rely largely on observational data from South Asia.

We summarized the risk factors, clinical manifestations, antifungal susceptibility patterns and treatment options for emerging uncommon moulds in Asia in Table 2.

TABLE 2.

Summary of risk factors, clinical manifestations, antifungal susceptibility patterns and preferred treatment options for emerging uncommon moulds reported predominantly in Asia.

Species	Risk factors	Clinical manifestations	Antifungal susceptibility patterns based on MIC testing	Preferred treatment options	References
Rhizopus homothallicus	Diabetic ketoacidosis	Pulmonary mucormycosis, cutaneous mucormycosis, rhinocerebral mucormycosis	MIC range Itraconazole (n = 34): 0.03–16 μg/mL Posaconazole (n = 34): 0.03–8 μg/mL Isavuconazole (n = 34): 0.03–16 μg/mL Amphotericin B (n = 34): 0.03–16 μg/mL Terbinafine (n = 34): 0.03–16 μg/mL	Amphotericin B, posaconazole	[98]
Schizophyllum commune	Normal host	Sinusitis, allergic bronchopulmonary mycosis, brain abscess	MIC range Itraconazole (n = 2): < 0.06–0.125 μg/mL Posaconazole (n = 2): 0.015–0.125 μg/mL Isavuconazole (n = 2): 0.125–0.25 μg/mL Amphotericin B (n = 2): 0.5–1.0 μg/mL MEC range Echinocandins (n = 2): 0.125–0.5 μg/mL	Itraconazole, voriconazole, posaconazole, amphotericin B	[125, 126]
Hormographiella aspergillata	Haematologic malignancies	Disseminated disease, endophthalmitis, infective endocarditis, pneumonia	MIC range Itraconazole (n = 11): 0.25 to ≥ 32 μg/mL Voriconazole (n = 9): 0.015–1 μg/mL Posaconazole (n = 6): 0.06–2 μg/mL Amphotericin B (n = 16): 0.03–32 μg/mL Micafungin (n = 9): 0.25 to ≥ 16 μg/mL	Voriconazole, amphotericin B	[127]
Volvariella volvacea	Haematologic malignancies, organ transplant recipient	Brain abscess, pulmonary infection, skin infection, infective endocarditis	MIC range Itraconazole (n = 2): 0.12–0.5 μg/mL Voriconazole (n = 2): 0.5–2.0 μg/mL Posaconazole (n = 2): 0.5–2.0 μg/mL Amphotericin B (n = 2): 0.5–2.0 μg/mL Echinocandins (n = 2): > 8 μg/mL	Voriconazole, amphotericin B	[128, 129]
Non‐marneffei Talaromyces	HIV infection, haematologic malignancies, chronic granulomatous disease	Pulmonary infection	MIC range for T. atroroseus: Itraconazole (n = 5): 0.12 to > 16 μg/mL Voriconazole (n = 5): 0.12 to > 8 μg/mL Posaconazole (n = 5): 0.25 to > 8 μg/mL Amphotericin B (n = 5): 0.5 to > 8 μg/mL Micafungin (n = 2): 0.12 to > 8 μg/mL	Should be based on susceptibility testing	[112]
Emergomyces spasteurianus	HIV infection, solid organ transplant recipients, diabetes mellitus, chronic kidney disease	Pulmonary infection, cutaneous infection, disseminated infection	MIC range for E. pasteurianus: Itraconazole (n = 5): 0.063–0.25 μg/mL Voriconazole (n = 5): 0.25 μg/mL Posaconazole (n = 5): 0.063–0.125 μg/mL Amphotericin B (n = 5): 0.031–0.125 μg/mL Micafungin (n = 2): 0.016–0.063 μg/mL	Amphotericin B induction followed by oral itraconazole	[130]
Trichophyton indotineae	Immunocompetent host	Severe dermatophytosis	MIC range Itraconazole (n = 16): 0.032–2 μg/mL Voriconazole (n = 5): 0.032–1 μg/mL Posaconazole (n = 5): 0.063–0.5 μg/mL Terbinafine (n = 16): 0.002 to ≥ 128 μg/mL Amphotericin B (n = 5): 2–4 μg/mL Micafungin (n = 2): < 0.001–0.032 μg/mL	Systemic itraconazole	[131]

Abbreviations: HIV, human immunodeficiency virus; MEC, minimal effective concentration; MIC, minimum inhibitory concentrations; n, number of isolates tested.

3.3. Pseudo‐Fungi

3.3.1. Oomycetes

Oomycetes are fungal‐like organisms classified within the class Oomycota. Two genera, Pythium and Lagenidium, are recognized causes of human infection [132]. Species of Pythium, most notably P. insidiosum, P. periculosum and P. aphanidermatum , are responsible for pythiosis [133], whereas lagenidiosis is caused primarily by L. giganteum and L. deciduum [134]. Pythiosis predominantly occurs in tropical and subtropical regions, including Thailand, Brazil and parts of the United States, and is typically associated with exposure to contaminated freshwater environments [135]. The disease manifests in several clinical forms. Vascular pythiosis represents the most severe presentation and is frequently observed in patients with underlying haematologic disorders, such as haemoglobinopathies or paroxysmal nocturnal haemoglobinuria (PNH) [136, 137]; ocular involvement, including keratitis and exogenous endophthalmitis, is more commonly reported in immunocompetent individuals [138, 139]. Cutaneous and subcutaneous pythiosis typically presents as chronic ulcerative lesions [140]. Diagnosis is often challenging because conventional cultures reveal hyaline, broad, non‐septate hyphae that closely resemble those seen in mucormycosis [141]. Ancillary diagnostic methods, including zoospore induction, molecular assays and serological testing, are essential for definitive identification [141, 142]. Surgical resection remains the cornerstone of management, with improved outcomes observed when combined with adjunctive antimicrobial therapy, such as azithromycin, doxycycline and itraconazole [143]. A study from Thailand demonstrated that residual disease following surgery was associated with significantly higher mortality compared with complete resection (31% vs. 15.7%), underscoring the critical importance of aggressive surgical management [143]. Serial monitoring of serum β‐d‐glucan levels may also be useful in assessing disease activity and treatment response [143].

Lagenidiosis is exceedingly rare in humans. First described in animals in the United States in 2003 [144], only a limited number of human cases have been reported, including cutaneous infection in a patient with acute myeloid leukaemia following haematopoietic stem cell transplantation after freshwater exposure [145] and a keratitis [146]. In culture, Lagenidium species grow rapidly on Sabouraud dextrose agar at 37°C, producing cream‐coloured, glabrous colonies [146]. Microscopic examination reveals broad, non‐septate hyphae with right‐angle branching, occasionally exhibiting coiling or vacuolation [146]. Zoospore induction can be achieved using boiled grass blades [142]. As with pythiosis, lagenidiosis may be misdiagnosed as mucormycosis based on histopathological features alone [146]. Definitive diagnosis requires molecular identification, typically through sequencing of the ITS and cytochrome oxidase subunit II (COXII) regions. Surgical intervention remains the mainstay of therapy, while antifungal options are limited; caspofungin and terbinafine have shown some activity, whereas azoles are generally ineffective due to the minimal ergosterol content of the oomycete cell membrane [146]. Much of the current evidence of human pythiosis and lagenidiosis originates from endemic countries, particularly Thailand, and consists primarily of retrospective cohorts and individual case reports. Improved clinician awareness and wider availability of molecular diagnostics will be essential to better define the epidemiology, optimize management, and improve outcomes.

3.4. Challenges in Antifungal Susceptibility Testing

Antifungal susceptibility testing has become increasingly important with the emergence of rare fungal pathogens exhibiting diverse intrinsic and acquired resistance mechanisms. However, antifungal susceptibility testing is evolving and translating in vitro susceptibility results into clinical decision‐making remains challenging. Although standardized antifungal susceptibility testing methodologies have been established in certain fungal pathogens, species‐specific clinical breakpoints are available for only a limited number of common yeasts and moulds [147] Consequently, for many emerging pathogens in this review, MIC values are unable to accurately categorize as susceptible, intermediate or resistant. Furthermore, epidemiological cutoff values (ECVs/ECOFFs) are lacking for most of these emerging organisms, making it difficult to distinguish wild‐type isolates from those harbouring acquired resistance mechanisms. Additional challenges arise from methodological differences, limited reproducibility for certain mould species, and the uncertain correlation between MIC values and clinical outcomes [148]. Some rare fungi also exhibit paradoxical growth, trailing effects or poor sporulation, further complicating susceptibility testing and interpretation [147]. As a result, antifungal susceptibility testing should not be interpreted in isolation but rather integrated with accurate species identification and clinical information.

These limitations highlight the urgent need for regional and global surveillance initiatives. Asia has emerged as a hotspot for several rare fungal pathogens, yet susceptibility data remain fragmented and are often derived from small, single‐centre studies. Large multicentre epidemiological studies are needed to define species distribution, establish regional MIC distributions, characterize emerging resistance mechanisms and correlate antifungal susceptibility testing with clinical outcomes. Strengthening laboratory capacity and establishing collaborative surveillance networks across Asia should therefore be considered a priority to improve the management of emerging rare fungal infections.

4. Conclusions

Rare fungi and fungal‐like pathogens represent an under‐recognized but clinically significant threat, particularly in resource‐limited settings. Their identification remains challenging due to nonspecific clinical presentations and morphological similarities with more common fungi, often necessitating advanced molecular techniques such as sequencing for definitive diagnosis. However, suboptimal laboratory infrastructure in many parts of Asia limits access to these tools, contributing to delays in accurate identification. Such delays can facilitate ongoing transmission, increase the risk of outbreaks and result in a higher burden of disease. Furthermore, the lack of established antifungal susceptibility breakpoints for many of these organisms complicates therapeutic decision‐making, frequently leading to suboptimal treatment. Collectively, these factors contribute to the persistently high mortality associated with infections caused by rare yeasts and moulds, underscoring the urgent need to strengthen diagnostic capacity, improve surveillance and develop standardized treatment guidelines.

Author Contributions

Narut Chancharussin: writing – review and editing, writing – original draft, methodology, conceptualization, data curation, formal analysis. Anupop Jitmuang: writing – review and editing, conceptualization, methodology, writing – original draft, validation, formal analysis. Arunaloke Chakrabarti: writing – review and editing, methodology, conceptualization, formal analysis. Methee Chayakulkeeree: writing – review and editing, conceptualization, supervision, methodology, validation, writing – original draft, formal analysis.

Funding

The authors have nothing to report.

Ethics Statement

The authors confirm that the ethical policies of the journal, as noted on the journal's author guidelines page, have been adhered to. No ethical approval was required as this is a review article with no original research data.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.