Airborne mould spores, including those of the Aspergillus species, are ubiquitous both indoors and outdoors. While they are generally harmless, inhaled spores can cause severe infections, particularly invasive pulmonary aspergillosis, in patients with impaired immune defences. Allergic manifestations such as asthma arise by different mechanisms and are not covered. This narrative mini-review summarises key evidence and guideline recommendations for healthcare teams and provides practical, patient-friendly advice by highlighting clinical and infection-prevention considerations. As there is no safe exposure threshold or minimum infectious dose for individual patients, prevention focuses on reducing avoidable exposure during high-risk periods. These high-risk periods typically refer to medical conditions such as prolonged neutropenia, the early post-transplant period, and high-dose corticosteroid therapy. Furthermore, prevention also focuses on optimising hospital environmental controls by implementing high-efficiency particulate air filter filtration, protective rooms and construction dust containment, alongside antifungal prophylaxis when indicated. The most impactful measures at home are preventing and rapidly remediating visible mould and dampness, avoiding high-spore activities such as composting, handling potting soil, and working with demolition or renovation dust, and maintaining simple hygiene practices that reduce dust reservoirs. This narrative mini-review also summarises what the literature can and cannot provide. Although Aspergillus species account for most of the available evidence, the same exposure-reduction principles apply to other environmentally acquired moulds, including Mucorales, Fusarium species and Scedosporium species.

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.

Pulmonary cryptococcosis (PC) in apparently immunocompetent hosts-now the majority of non-HIV cases in Asia-cannot be explained by the traditional opportunistic infection paradigm. Three epidemiological observations point toward occult immune susceptibility: familial clustering documented in multiple case reports and small family studies despite shared environmental exposure, normal routine immunological screening, and species-specific infection patterns between Cryptococcus neoformans and Cryptococcus gattii. We propose a three-layer framework: upstream genetic variants in pattern recognition, Fcγ receptor, complement-lectin, and macrophage-regulatory loci (Layer 1) act in concert with intermediate immune phenotypes (Layer 2)-the genetically influenced IL-17/Th17 axis and IgG2 subclass deficiencies, and acquired anti-GM-CSF neutralising autoantibodies-that are proposed to converge on alveolar macrophage dysfunction and defective pulmonary fungal clearance (Layer 3). The three Layer 2 phenotypes differ substantially in evidence strength: anti-GM-CSF autoantibodies have reached clinical validation; IgG2 deficiency remains a mechanistic hypothesis; and IL-17/Th17 deficiency is supported by a single unreplicated study and should be treated as preliminary. This framework is hypothesis-generating, derived from candidate-gene studies, limited immunophenotyping data, and animal models; it has not been validated by genome-wide association studies or prospective functional research, and its clinical value requires confirmation by higher-quality evidence.