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Fungal infection
Fungal infection
Fungal infection
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Mycosis
Other namesMycoses,[1] fungal disease,[2] fungal infection[3]
ICD-10CM codes: Mycoses B35-B49 [4]
Micrograph showing a mycosis (aspergillosis). The Aspergillus (which is spaghetti-like) is seen in the center and surrounded by inflammatory cells and necrotic debris. H&E stain.
SpecialtyInfectious Diseases[5]
TypesSystemic, superficial, subcutaneous[3]
CausesPathogenic fungus: dermatophytes, yeasts, molds[6][7]
Risk factorsImmunodeficiency, cancer treatment, large surface area wounds/burns,[8][9] organ transplant,[6] COVID-19,[10] tuberculosis
Diagnostic methodBased on symptoms, culture, microscopic examination[6]
TreatmentAntifungals[3]
FrequencyCommon[11]
Deaths1.7 million (2020)[12]

Fungal infection, also known as mycosis, is a disease caused by fungi.[5][13] Different types are traditionally divided according to the part of the body affected: superficial, subcutaneous, and systemic.[3][6] Superficial fungal infections include common tinea of the skin, such as tinea of the body, groin, hands, feet and beard, and yeast infections such as pityriasis versicolor.[7] Subcutaneous types include eumycetoma and chromoblastomycosis, which generally affect tissues in and beneath the skin.[1][7] Systemic fungal infections are more serious and include cryptococcosis, histoplasmosis, pneumocystis pneumonia, aspergillosis and mucormycosis.[3] Signs and symptoms range widely.[3] There is usually a rash with superficial infection.[2] Fungal infection within the skin or under the skin may present with a lump and skin changes.[3] Pneumonia-like symptoms or meningitis may occur with a deeper or systemic infection.[2]

Fungi are everywhere, but only some cause disease.[13] Fungal infection occurs after spores are either breathed in, come into contact with skin or enter the body through the skin such as via a cut, wound or injection.[3] It is more likely to occur in people with a weak immune system.[14] This includes people with illnesses such as HIV/AIDS, and people taking medicines such as steroids or cancer treatments.[14] Fungi that cause infections in people include yeasts, molds and fungi that are able to exist as both a mold and yeast.[3] The yeast Candida albicans can live in people without producing symptoms, and is able to cause both superficial mild candidiasis in healthy people, such as oral thrush or vaginal yeast infection, and severe systemic candidiasis in those who cannot fight infection themselves.[3]

Diagnosis is generally based on signs and symptoms, microscopy, culture, sometimes requiring a biopsy and the aid of medical imaging.[6] Some superficial fungal infections of the skin can appear similar to other skin conditions such as eczema and lichen planus.[7] Treatment is generally performed using antifungal medicines, usually in the form of a cream or by mouth or injection, depending on the specific infection and its extent.[15] Some require surgically cutting out infected tissue.[3]

Fungal infections have a world-wide distribution and are common, affecting more than one billion people every year.[11] An estimated 1.7 million deaths from fungal disease were reported in 2020.[12] Several, including sporotrichosis, chromoblastomycosis and mycetoma are neglected.[16]

A wide range of fungal infections occur in other animals, and some can be transmitted from animals to people.[17]

Classification

[edit]

Mycoses are traditionally divided into superficial, subcutaneous, or systemic, where infection is deep, more widespread and involving internal body organs.[3][11] They can affect the nails, vagina, skin and mouth.[18] Some types such as blastomycosis, cryptococcus, coccidioidomycosis and histoplasmosis, affect people who live in or visit certain parts of the world.[18] Others such as aspergillosis, pneumocystis pneumonia, candidiasis, mucormycosis and talaromycosis, tend to affect people who are unable to fight infection themselves.[18] Mycoses might not always conform strictly to the three divisions of superficial, subcutaneous and systemic.[3] Some superficial fungal infections can cause systemic infections in people who are immunocompromised.[3] Some subcutaneous fungal infections can invade into deeper structures, resulting in systemic disease.[3] Candida albicans can live in people without producing symptoms, and is able to cause both mild candidiasis in healthy people and severe invasive candidiasis in those who cannot fight infection themselves.[3][7]

ICD-11 codes

[edit]

ICD-11 codes include:[5]

Superficial mycoses

[edit]

Superficial mycoses include candidiasis in healthy people, common tinea of the skin, such as tinea of the body, groin, hands, feet and beard, and malassezia infections such as pityriasis versicolor.[3][7]

  • Oral candidiasis
    Oral candidiasis
  • Tinea corporis
    Tinea corporis
  • Pityriasis versicolor
    Pityriasis versicolor
  • Onychomycosis
    Onychomycosis

Subcutaneous

[edit]
Eumycetoma

Subcutaneous fungal infections include sporotrichosis, chromoblastomycosis, and eumycetoma.[3]

Systemic

[edit]

Systemic fungal infections include histoplasmosis, cryptococcosis, coccidioidomycosis, blastomycosis, mucormycosis, aspergillosis, pneumocystis pneumonia and systemic candidiasis.[3]

Systemic mycoses due to primary pathogens originate normally in the lungs and may spread to other organ systems. Organisms that cause systemic mycoses are inherently virulent.[further explanation needed].[citation needed] Systemic mycoses due to opportunistic pathogens are infections of people with immune deficiencies who would otherwise not be infected. Examples of immunocompromised conditions include AIDS, alteration of normal flora by antibiotics, immunosuppressive therapy, and metastatic cancer. Examples of opportunistic mycoses include Candidiasis, Cryptococcosis and Aspergillosis.[citation needed]

Signs and symptoms

[edit]

Most common mild mycoses often present with a rash.[2] Infections within the skin or under the skin may present with a lump and skin changes.[3] Less common deeper fungal infections may present with pneumonia-like symptoms or meningitis.[2]

Causes

[edit]

Mycoses are caused by certain fungi; yeasts, molds and some fungi that can exist as both a mold and yeast.[3][6] They are everywhere and infection occurs after spores are either breathed in, come into contact with skin or enter the body through the skin such as via a cut, wound or injection.[3] Candida albicans is the most common cause of fungal infection in people, particularly as oral or vaginal thrush, often following taking antibiotics.[3]

Risk factors

[edit]

Fungal infections are more likely in people with weak immune systems.[14] This includes people with illnesses such as HIV/AIDS, and people taking medicines such as steroids or cancer treatments.[14] People with diabetes also tend to develop fungal infections.[19] Very young and very old people, also, are groups at risk.[20]

Individuals being treated with antibiotics are at higher risk of fungal infections.[21]

Children whose immune systems are not functioning properly (such as children with cancer) are at risk of invasive fungal infections.[22]

COVID-19

[edit]

During the COVID-19 pandemic some fungal infections have been associated with COVID-19.[10][23][24] Fungal infections can mimic COVID-19 and occur at the same time as COVID-19, and more serious fungal infections can complicate COVID-19.[10] A fungal infection may occur after antibiotics for a bacterial infection which has occurred following COVID-19.[25] The most common serious fungal infections in people with COVID-19 include aspergillosis and invasive candidiasis.[26] COVID-19–associated mucormycosis is generally less common, but in 2021 was noted to be significantly more prevalent in India.[10][27]

Mechanism

[edit]

Fungal infections occur after spores are breathed in, come into contact with skin or enter the body through a wound.[3]

Diagnosis

[edit]
Workup algorithm of fungal infection at a microbiology lab at a New England community hospital.

Diagnosis is generally by signs and symptoms, microscopy, biopsy, culture and sometimes with the aid of medical imaging.[6]

Differential diagnosis

[edit]

Some tinea and candidiasis infections of the skin can appear similar to eczema and lichen planus.[7] Pityriasis versicolor can look like seborrheic dermatitis, pityriasis rosea, pityriasis alba and vitiligo.[7]

Some fungal infections such as coccidioidomycosis, histoplasmosis, and blastomycosis can present with fever, cough, and shortness of breath, thereby resembling COVID-19.[28]

Prevention

[edit]

Keeping the skin clean and dry, as well as maintaining good hygiene, will help larger topical mycoses. Because some fungal infections are contagious, it is important to wash hands after touching other people or animals. Sports clothing should also be washed after use.[clarification needed][citation needed]

Treatment

[edit]

Treatment depends on the type of fungal infection, and usually requires topical or systemic antifungal medicines.[15] Pneumocystosis that does not respond to anti-fungals is treated with co-trimoxazole.[29] Sometimes, infected tissue needs to be surgically cut away.[3]

Epidemiology

[edit]

Worldwide, every year fungal infections affect more than one billion people.[11] An estimated 1.6 million deaths from fungal disease were reported in 2017.[30] The figure has been rising, with an estimated 1.7 million deaths from fungal disease reported in 2020.[12] Fungal infections also constitute a significant cause of illness and mortality in children.[31]

According to the Global Action Fund for Fungal Infections, every year there are over 10 million cases of fungal asthma, around 3 million cases of long-term aspergillosis of lungs, 1 million cases of blindness due to fungal keratitis, more than 200,000 cases of meningitis due to cryptococcus, 700,000 cases of invasive candidiasis, 500,000 cases of pneumocystosis of lungs, 250,000 cases of invasive aspergillosis, and 100,000 cases of histoplasmosis.[32]

History

[edit]

In 500 BC, an account of ulcers in the mouth by Hippocrates may have described thrush.[33] Paris-based Hungarian microscopist David Gruby first reported that human disease could be caused by fungi in the early 1840s.[33]

SARS 2003

[edit]

During the 2003 SARS outbreak, fungal infections were reported in 14.8–33% of people affected by SARS, and it was the cause of death in 25–73.7% of people with SARS.[34]

Other animals

[edit]

A wide range of fungal infections occur in other animals, and some can be transmitted from animals to people, such as Microsporum canis from cats.[17]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Fungal infection

View on Grokipedia
from Grokipedia
Fungal infections, also known as mycoses, are diseases caused by pathogenic fungi, a diverse group of eukaryotic microorganisms that include yeasts, molds, and mushroom-like organisms. These infections can manifest as superficial conditions affecting the skin, , or , or as invasive systemic illnesses involving the lungs, bloodstream, or other internal organs, ranging from mild and self-limiting to severe and potentially fatal, particularly in individuals with weakened immune systems. Fungi are ubiquitous in the environment, thriving in soil, air, water, plants, and even as normal flora on or in the human body, where they typically remain harmless. Infections arise when fungal spores are inhaled, enter through breaks in the skin, or overgrow opportunistically, often triggered by factors such as antibiotic use, diabetes, or immunosuppression from conditions like HIV/AIDS, organ transplants, or chemotherapy. People with intact immune systems may experience only mild infections, while those at higher risk face greater severity and complications. Common types of fungal infections include superficial dermatophytoses such as ringworm (tinea corporis), athlete's foot (tinea pedis), and jock itch (tinea cruris), which cause itchy, scaly rashes on the skin; onychomycosis, leading to thickened, discolored nails; and candidiasis, manifesting as oral thrush or vaginal yeast infections with white patches or discharge. More serious endemic or opportunistic infections encompass histoplasmosis and coccidioidomycosis (valley fever), which primarily affect the lungs after inhaling spores in specific geographic areas, and invasive forms like aspergillosis, cryptococcosis, or candidemia, which can disseminate to cause pneumonia, meningitis, or sepsis in hospitalized or immunocompromised patients. Symptoms depend on the infection site and type but frequently involve localized itching, redness, and scaling for and nail issues, or systemic signs like fever, , , fatigue, and for pulmonary or disseminated cases. typically requires microscopic examination, culture, or molecular tests, while treatment relies on agents: topical azoles or allylamines for superficial infections, and systemic options like , echinocandins, or for invasive disease, though emerging resistance complicates management. Fungal diseases represent a growing burden, with an estimated 2.5 million attributable deaths annually from severe cases (as of ), underscoring the need for improved prevention through awareness, hygiene, and avoiding high-risk environments.

Classification

Superficial mycoses

Superficial mycoses are fungal infections confined to the outermost layers of the skin, hair, and nails, specifically the and keratinized structures, without invasion into deeper tissues or elicitation of significant . These infections are typically benign and localized, contrasting with systemic mycoses that can disseminate to internal organs. The primary causative agents include dermatophytes from the genera Trichophyton, Microsporum, and Epidermophyton, which have a strong affinity for and are responsible for most tinea infections. Other key pathogens are yeasts such as species (e.g., M. globosa and M. furfur), which cause pityriasis versicolor, and Candida species, which can contribute to in certain cases. Less common agents include for black piedra and Trichosporon species for , affecting hair shafts. Key examples encompass tinea infections, such as (ringworm), characterized by annular scaly patches on the body; tinea pedis (), involving interdigital scaling and maceration; and (jock itch), presenting as pruritic erythematous plaques in the . refers to nail infections leading to discoloration, thickening, and brittleness, often caused by . versicolor manifests as hypo- or hyperpigmented macules on the trunk and proximal extremities due to overgrowth. Transmission occurs primarily through direct contact with infected humans or animals, indirect contact via fomites like towels or clothing, or environmental sources such as soil harboring geophilic dermatophytes. These infections are not highly contagious in all cases, as -related conditions arise from commensal flora under favorable conditions rather than person-to-person spread. is estimated at 20-25% globally, with higher rates in tropical and subtropical climates due to warmth and humidity promoting fungal growth, and among athletes owing to occlusive and creating moist environments. In tropical regions, pityriasis versicolor can affect up to 50% of the population, particularly adolescents and young adults.

Subcutaneous mycoses

Subcutaneous mycoses are fungal infections that involve the , subcutaneous fat, and occasionally adjacent structures such as , typically arising from traumatic of environmental fungi into the skin. These infections are chronic and localized, distinguishing them from more superficial or disseminated forms, and are prevalent in tropical and subtropical regions where exposure to soil and vegetation is common. The primary causative agents include dimorphic fungi such as , which causes , and dematiaceous (pigmented) molds like Fonsecaea pedrosoi and Cladophialophora carrionii for , Madurella mycetomatis for , and various dematiaceous species (e.g., Exophiala spp.) for phaeohyphomycosis. These organisms are ubiquitous in , decaying wood, and matter but have low , requiring a breach in the skin barrier to establish infection. Key examples illustrate the diversity of these infections. , often termed "rose gardener's disease," manifests as fixed cutaneous nodules or lymphocutaneous chains of ulcerated lesions following inoculation from thorns or splinters. presents with slowly enlarging, verrucous plaques or cauliflower-like growths on the lower extremities, characterized by sclerotic bodies in tissue. (fungal mycetoma) develops as painless subcutaneous swellings with sinus tracts discharging grains, potentially leading to bone destruction if untreated. Phaeohyphomycosis appears as abscesses, cysts, or granulomas with pigmented hyphae visible histologically, often mimicking bacterial infections. Transmission occurs primarily through traumatic inoculation, such as cuts, punctures, or abrasions contaminated by , , or decaying organic material; person-to-person spread is exceedingly rare. In some cases, like zoonotic in , scratches from infected cats can serve as a vector. Clinically, these infections progress slowly over months to years, starting with a small or nodule at the inoculation site that evolves into granulomatous, ulcerative, or suppurative lesions; lymphatic spread may produce beaded chains of nodules, while deeper invasion can form abscesses or fistulas without systemic dissemination in immunocompetent hosts. may exacerbate progression, though details on risk factors are covered elsewhere.

Systemic mycoses

Systemic mycoses refer to disseminated fungal infections that spread via the bloodstream or lymphatics to internal organs such as the lungs, , and other viscera, often resulting in severe, life-threatening disease particularly in immunocompromised individuals. These infections are characterized by their opportunistic nature, where fungi that are typically environmental saprophytes invade susceptible hosts, leading to high mortality rates if untreated. Unlike superficial or subcutaneous infections, systemic mycoses involve multi-organ dissemination and are primarily caused by fungi with inherent or those exploiting host immune defects. The primary causative agents include thermally dimorphic fungi, which exist as molds in the environment and convert to yeast forms at , such as Histoplasma capsulatum, Blastomyces dermatitidis, and Coccidioides immitis/posadasii. Opportunistic pathogens, including molds like Aspergillus species and yeasts such as Cryptococcus neoformans and Pneumocystis jirovecii, also drive these infections, particularly in hosts with impaired immunity. Additionally, Mucorales fungi (e.g., Rhizopus and Mucor species) contribute to through angioinvasive growth. Transmission typically occurs through of fungal spores or microconidia from contaminated environmental sources, such as enriched with or in endemic regions. For dimorphic fungi, exposure is geographically restricted; for instance, H. capsulatum is prevalent in the and valleys. Reactivation of latent infections can also precipitate dissemination in immunocompromised states, without new environmental exposure. Key examples illustrate the clinical spectrum. , caused by H. capsulatum, often begins as a primary pulmonary following but can disseminate to the in AIDS patients, causing fever, , and organ involvement. , due to B. dermatitidis, similarly starts in the lungs via in endemic areas like the southeastern and , progressing to widespread dissemination in immunocompromised hosts. (C. immitis/posadasii) is acquired by inhaling arthroconidia in arid regions such as the , manifesting as primary or severe extrapulmonary disease in vulnerable individuals. , from C. neoformans, spreads hematogenously after pulmonary entry, frequently causing in AIDS patients with counts below 100 cells/μL. , primarily A. fumigatus, invades via inhaled conidia and causes invasive pulmonary or disseminated disease in transplant recipients, with high risk in the early posttransplant period. involves rapid angioinvasion by Mucorales, often presenting as pulmonary or rhinocerebral in immunocompromised or diabetic patients following . These forms—primary pulmonary, disseminated, and opportunistic—highlight the infections' adaptability to host vulnerabilities.

Nomenclature and coding

The nomenclature of fungal infections has evolved significantly from early descriptive terms, such as "ringworm" for dermatophytoses, which were based on visible clinical manifestations, to a more systematic approach in the 19th and early 20th centuries relying on morphological characteristics like shape and hyphal structure for . This morphological , formalized through works like those of Pier Antonio Micheli and later mycologists, grouped fungi into genera such as and Candida based on microscopic features. By the late 20th century, advances in shifted the paradigm toward genetic methods, with (ITS) sequencing of becoming the gold standard for fungal identification since the 1990s, enabling precise delineation of species complexes previously indistinguishable by morphology alone. In the International Classification of Diseases, 11th Revision (ICD-11), fungal infections are categorized under Chapter 1 (Certain infectious or parasitic diseases), block 1F2 (Mycoses), which encompasses specific codes for various infection types rather than broad subdivisions by depth of involvement. Superficial mycoses, such as dermatophytoses, are coded under 1F28 (e.g., 1F28.2 for tinea pedis, or athlete's foot), while subcutaneous mycoses fall under codes like 1F24 (chromoblastomycosis) and 1F29 (eumycetoma). Systemic mycoses are represented by codes including 1F20 (aspergillosis), 1F23 (candidosis), and 1F2A (histoplasmosis), facilitating standardized reporting across healthcare systems. Other classification systems complement for clinical documentation; for instance, provides detailed terminology for fungal infections, with the root concept "Mycosis (disorder)" coded as 3218000, and subtypes like "Invasive fungal infection (disorder)" under 12391000132109, enabling granular electronic health record integration. Additionally, the World Health Organization's 2022 Fungal Priority Pathogens List (FPPL) identifies critical threats, including Candida auris, , , and , to prioritize research and surveillance efforts. Standardized and coding are crucial for epidemiological , as they enable consistent tracking of incidence, outbreaks, and resistance patterns, such as azole-resistant Aspergillus fumigatus strains, which have emerged globally due to environmental and clinical pressures, informing responses and resource allocation. This framework supports global reporting systems, reducing misclassification and enhancing the detection of emerging threats like multidrug-resistant fungi.

Clinical features

Signs and symptoms

Fungal infections manifest with diverse that vary by infection depth and location, often reflecting the host's immune response to fungal invasion. Superficial infections, affecting the skin, , or , typically present with localized itching, scaling, redness, or , such as the annular rashes seen in dermatophytoses. Subcutaneous infections commonly elicit chronic inflammatory responses, including granulomatous reactions, abscesses, nodules, and ulcerative lesions along lymphatic channels or at implantation sites. , pustules, and swelling may accompany these as part of the acute inflammatory process in affected tissues. Systemic infections often involve constitutional signs like fever, , and , alongside organ-specific effects; pulmonary involvement can cause and dyspnea, while central nervous system spread may lead to , altered mental status, or meningitis-like symptoms. Progression from acute to chronic forms is indicated by persistent symptoms or dissemination, such as the appearance of multifocal skin lesions signaling bloodstream involvement in . Some fungal colonizations remain asymptomatic, particularly mucosal carriage of Candida species in healthy individuals, where no clinical disease develops despite fungal presence. In immunocompromised hosts, however, risk factors like can exacerbate symptom severity and promote rapid dissemination.

Specific manifestations by infection type

Fungal infections manifest differently depending on whether they are superficial, subcutaneous, or systemic, with distinct clinical presentations that guide and . Superficial mycoses primarily affect the skin, hair, and nails without deeper tissue invasion, often presenting as localized, non-life-threatening lesions. In tinea infections, such as , characteristic annular rashes with scaly, erythematous borders and central clearing are common, typically on the trunk or extremities. versicolor, caused by species, appears as hypopigmented or hyperpigmented patches with fine scaling, predominantly on the upper trunk and neck, exacerbated by heat and humidity. involves nail discoloration, often yellow-white or brown, accompanied by thickening and brittleness, most frequently affecting toenails. Subcutaneous mycoses arise from traumatic implantation of fungi into deeper skin layers, leading to chronic, localized inflammatory responses. commonly presents as lymphocutaneous nodules, starting with a painless at the site that progresses to a chain of ulcerated nodules along lymphatic channels, often on the arms in gardeners or farmers. features verrucous plaques with hyperkeratotic, cauliflower-like surfaces, typically on the lower extremities, evolving slowly over years with potential for secondary bacterial . Mycetoma is characterized by sinus tracts discharging grains (colonies of the causative ), along with swelling and abscesses, usually on the feet in endemic regions. Systemic mycoses involve dissemination via bloodstream or , affecting internal organs and often requiring prompt intervention. In , chronic pulmonary forms show cavitary lung lesions on imaging, with symptoms like and in endemic areas such as the Ohio River Valley. (valley fever) typically presents with pulmonary symptoms including fatigue, , fever, , , night sweats, and a on the upper body or legs, primarily after in arid regions like the . Invasive often manifests as fever, , (sometimes with ), and in immunocompromised patients, with potential for invasive lung disease or dissemination. Disseminated candidiasis may produce multiple skin papules or nodules, resembling septic emboli, in addition to fever and organ involvement, particularly in hospitalized patients. frequently causes with , fever, and altered mental status, detectable via analysis, though pulmonary nodules can precede central nervous system spread. Manifestations vary significantly by host immune status; in immunocompetent individuals, infections are often self-limited or mild, confined to superficial or localized sites, whereas immunocompromised hosts, such as those with or , experience severe dissemination with higher mortality. For instance, in HIV patients progresses rapidly to , unlike the asymptomatic pulmonary form in healthy hosts, and in diabetics leads to invasive disease with poor outcomes due to impaired function. Rare manifestations include from Candida, presenting as vitreous inflammation and vision loss in endogenous spread from bloodstream infections, and orbital involvement in , with proptosis, ophthalmoplegia, tissue , facial swelling, and black nasal , particularly in diabetic or neutropenic patients and increasingly associated with as of 2025. These uncommon presentations underscore the need for vigilance in at-risk populations.

Etiology

Causative agents

Fungal infections, or mycoses, are primarily caused by fungi belonging to three major groups: , molds, and dimorphic fungi. are unicellular fungi that reproduce by budding, with being the most common opportunistic responsible for in humans. Another key is , which primarily affects immunocompromised individuals and causes through inhalation of spores. Molds are multicellular, filamentous fungi that grow as hyphae and produce asexual spores called conidia, which serve as infectious propagules; notable examples include , a ubiquitous mold causing , and Rhizopus spp., which lead to in susceptible hosts. Dimorphic fungi exhibit thermal dimorphism, growing as molds at environmental temperatures (around 25°C) and switching to or spherule forms at (37°C), facilitating tissue invasion; is a prototypical dimorphic causing . These pathogens possess distinct characteristics that contribute to their infectivity. Many molds and dimorphic fungi produce conidia as lightweight, airborne spores for dissemination, while arthroconidia—formed by hyphal fragmentation—are characteristic of dermatophytes like Trichophyton spp. and the dimorphic fungus . Thermal dimorphism enables environmental survival and host adaptation in pathogens such as and Paracoccidioides brasiliensis. Yeasts like Candida species form biofilms, structured communities embedded in an that enhance adherence to surfaces and resistance to antifungals. Emerging and regionally restricted agents highlight the evolving threat of fungal pathogens. Candida auris, a multidrug-resistant yeast first identified in 2009 in , has rapidly spread globally, causing invasive infections in healthcare settings with high mortality rates. In , the dimorphic fungus Talaromyces marneffei (formerly marneffei) is a significant opportunistic , particularly among patients, causing disseminated talaromycosis. Fungal pathogens reside in specific environmental reservoirs that facilitate human exposure. Dermatophytes, such as and species, are keratophilic fungi primarily found in , where they degrade , as well as on animal hosts. thrives in nitrogen-rich soils contaminated with bird or bat , particularly in river valleys of the . species, opportunistic molds causing fusariosis, are ubiquitous in , debris, and aquatic environments like water distribution systems. Virulence factors enable these fungi to colonize and invade hosts. Adhesins, such as the family proteins in , mediate attachment to host cells and surfaces. Secreted enzymes, including phospholipases in Candida species, degrade host membranes to promote tissue penetration and nutrient acquisition.

Risk factors

Individuals with compromised immune systems are at heightened risk for fungal infections due to impaired ability to combat opportunistic pathogens. Conditions such as significantly increase susceptibility, particularly when + lymphocyte counts fall below 200 cells/mm³, elevating the risk of pneumonia (PCP). Chemotherapy-induced and immunosuppressive therapies following organ or stem cell transplants further predispose patients by suppressing innate and adaptive immune responses. use, common in transplant recipients and , exacerbates this vulnerability by altering immune cell function and promoting fungal proliferation. Comorbidities play a critical role in predisposing individuals to specific fungal infections. Uncontrolled diabetes mellitus, especially with or , is a major risk factor for , accounting for 54-76% of cases in affected populations. Chronic lung diseases, such as (COPD) or , increase the likelihood of invasive pulmonary by providing a conducive environment for colonization and invasion. Iatrogenic factors arising from medical interventions contribute substantially to fungal infection risks. therapy disrupts the normal , facilitating overgrowth and dissemination of Candida species, leading to candidemia. Indwelling central venous catheters and invasive procedures, such as or , create portals of entry for fungi and heighten nosocomial rates. Environmental exposures represent another key vulnerability, particularly for endemic mycoses. Occupational activities involving soil disturbance, such as farming or in the , expose workers to arthroconidia, increasing incidence among agricultural laborers. Travel to or residence in endemic regions, including arid areas of the for or the Ohio-Mississippi River valleys for , heightens acquisition risk through inhalation of fungal spores during outdoor activities. Recent developments have highlighted emerging risks associated with viral pandemics and therapeutic resistance. A surge in cases occurred in from 2020 to 2023, linked to widespread use (e.g., dexamethasone) for management, particularly in patients with poorly controlled , resulting in rates up to 80 times higher than in developed countries. resistance is an evolving concern, as pathogens like Candida auris and species develop resistance to azoles and echinocandins, complicating treatment and amplifying risks in vulnerable populations.

Pathogenesis

Mechanisms of infection

Fungal infections typically initiate through specific entry portals that allow opportunistic or environmental fungi to access host tissues. The primary routes include of airborne spores, which predominantly targets the and can lead to systemic mycoses such as or ; traumatic injury to the skin, facilitating subcutaneous infections like ; and disruption of mucosal barriers, as seen in oropharyngeal where endogenous flora like exploits local imbalances. These portals are often compromised in individuals with risk factors such as or chronic lung disease, though detailed risk profiles are outlined elsewhere. Once at the entry site, fungi employ adhesion mechanisms to colonize host surfaces, utilizing specialized adhesins—surface proteins that bind to epithelial cells or extracellular matrix components. For instance, in Candida albicans, the ALS family of adhesins mediates attachment to mucosal epithelia, enabling initial colonization before progression to deeper tissues. Adhesion is followed by invasion, where fungi secrete hydrolytic enzymes to penetrate host barriers; hyphal forms of C. albicans release secreted aspartyl proteinases (Saps) that degrade epithelial proteins, allowing direct penetration and tissue damage. Similarly, in Aspergillus fumigatus, rodlet proteins like RodA contribute to adhesion on lung epithelia, while enzymes such as elastases facilitate hyphal invasion of alveolar walls. Spore germination represents a critical transition in many fungal pathogens, triggered by host environmental cues that promote morphological adaptation. In dimorphic fungi like , inhaled conidia germinate in the warm, humid conditions of the lungs (around 37°C), shifting from mold to yeast phase to evade clearance and establish infection. This temperature-induced dimorphic switch is regulated by signaling pathways involving cAMP and MAPK cascades, enhancing survival within alveolar macrophages. Environmental factors such as pH and nutrient availability further modulate germination in pathogens like , where arthroconidia develop into spherules upon inhalation. Biofilm formation provides fungi with a protective niche, particularly on indwelling medical devices such as catheters, where communities of adherent cells resist clearance. In Candida species, biofilms develop in sequential stages—adhesion of yeast cells, followed by hyphal proliferation and extracellular matrix production—creating a barrier that shields against phagocytosis and antifungal agents. This architecture reduces susceptibility to host defenses by limiting immune cell access and altering fungal metabolism, as observed in device-related candidemia. Certain fungi establish latency after initial , remaining dormant until host conditions favor reactivation. In Histoplasma capsulatum, yeast forms persist intracellularly within lung , entering a quiescent state that can last years; , such as from or corticosteroids, disrupts granuloma integrity, allowing fungal proliferation and dissemination. This reactivation mechanism underscores the pathogen's ability to exploit waning immunity for disease re-emergence.

Host-pathogen interactions

Host-pathogen interactions in fungal infections involve a dynamic interplay between the host's immune system and the pathogen's survival strategies, primarily mediated through innate and adaptive immune responses. Innate immunity serves as the first line of defense, with macrophages and neutrophils playing critical roles in phagocytosing fungal yeasts and hyphae. These phagocytes recognize fungal cell wall components, such as beta-glucan, via pattern recognition receptors including Toll-like receptors (TLRs), particularly TLR2 and TLR4, which trigger inflammatory cascades to limit pathogen dissemination. For instance, dectin-1, a C-type lectin receptor, binds beta-glucan to activate downstream signaling for phagocytosis and cytokine production, enhancing antifungal activity against pathogens like Candida albicans. Adaptive immunity complements innate responses, with T-cell mediated immunity being essential for controlling dimorphic fungi such as . + T cells, particularly Th1 and Th17 subsets, produce interferon-gamma (IFN-γ) and interleukin-17 (IL-17), which activate macrophages and recruit neutrophils to clear intracellular fungi. Antibody responses are often limited by fungal polysaccharide capsules, as seen in , where the capsule masks antigens and inhibits effective opsonization, reducing B-cell driven . Fungal pathogens employ sophisticated evasion tactics to subvert host defenses, including the production of capsules that inhibit , as exemplified by the cryptococcal capsule which also suppresses T-cell proliferation. Siderophores enable iron acquisition from the host, allowing pathogens like to thrive in iron-restricted environments by chelating iron from . Additionally, toxins such as gliotoxin produced by impair immune cell function by inducing in neutrophils and macrophages, further promoting fungal persistence. These interactions often culminate in tissue pathology, where excessive immune activation leads to cytokine storms involving elevated levels of pro-inflammatory cytokines like tumor factor-alpha (TNF-α) and IL-6 in severe invasive , exacerbating organ damage. In , angioinvasion by species causes endothelial damage, , and subsequent tissue due to vascular occlusion and fungal hyphal penetration. Host genetic factors significantly influence susceptibility to these interactions, with polymorphisms in the CARD9 gene impairing signaling from receptors and increasing vulnerability to invasive fungal infections such as chronic mucocutaneous candidiasis and deep dermatophytosis. CARD9 mutations disrupt Th17 responses, leading to defective IL-17 production and impaired fungal clearance, as observed in patients with homozygous loss-of-function variants.

Diagnosis

Diagnostic methods

Diagnosis of fungal infections relies on a combination of direct and indirect techniques, as well as modalities, to confirm the presence and identify the causative . Direct methods, such as and , provide rapid visualization or isolation of fungi from clinical specimens, while indirect approaches like molecular assays, , and detection offer higher specificity for identification, particularly in invasive cases. These methods are essential due to the often nonspecific clinical presentation of fungal infections and the need for timely intervention in at-risk populations. Microscopy remains a cornerstone for initial rapid diagnosis, allowing direct examination of fungal elements in specimens. (KOH) wet mount preparation is commonly used for skin scrapings, nail clippings, or hair samples in superficial infections like , where it dissolves to reveal hyphae or spores under light . For , particularly in (CSF), staining highlights the capsule surrounding yeast cells, producing a characteristic that aids presumptive identification. These techniques are cost-effective and provide immediate results but require expertise for accurate interpretation and cannot speciate fungi. Fungal culture enables definitive isolation and identification of pathogens from clinical samples such as blood, tissue, or respiratory secretions. Sabouraud dextrose agar is a standard medium for primary isolation, supporting the growth of most fungi at while inhibiting bacterial overgrowth through its low and additives. Once grown, identification relies on macroscopic and microscopic morphology, such as colony characteristics and formation, or advanced methods like (MALDI-TOF MS), which analyzes protein profiles for rapid, accurate species-level detection of molds and yeasts. Culture remains the gold standard for susceptibility testing but can take days to weeks, limiting its utility in acute settings. Molecular techniques have revolutionized fungal diagnostics by enabling sensitive detection of fungal DNA or RNA in diverse specimens. Polymerase chain reaction (PCR) assays targeting conserved regions like the pan-fungal 18S rRNA gene allow broad-spectrum identification of fungi, including those that are difficult to culture, with real-time formats providing quantitative results for monitoring disease burden. Antigen-based tests complement PCR; for instance, galactomannan detection in serum or bronchoalveolar lavage fluid is specific for invasive aspergillosis, while (1→3)-β-D-glucan assays detect cell wall components common to many invasive fungi, aiding early diagnosis in immunocompromised patients. These methods offer high specificity (often >90%) but may require specialized equipment and can be affected by prior antifungal therapy. Serologic tests detect host immune responses or fungal antigens, proving valuable for endemic mycoses. In histoplasmosis, enzyme immunoassay (EIA) for urine Histoplasma antigen is highly sensitive (>90%) for disseminated disease, allowing noninvasive diagnosis, while complement fixation or immunodiffusion assays detect IgG antibodies in serum to support chronic or past infections. These assays are particularly useful in regions where Histoplasma capsulatum is prevalent, though cross-reactivity with other fungi necessitates confirmatory testing. Imaging plays a supportive role in localizing infections and guiding biopsies, though it is not specific to fungi. Computed tomography (CT) scans are preferred for pulmonary manifestations, revealing nodules, cavities, or halo signs suggestive of in endemic areas like the . (MRI) excels in (CNS) involvement, such as , where it delineates abscesses or vascular invasion with contrast enhancement. Tissue with histopathologic examination, often using Gomori methenamine silver (GMS) stain, confirms fungal elements like spherules in or septate hyphae in , providing morphologic evidence of invasion. Recent advances address limitations of traditional methods, particularly for unculturable or mixed infections. Next-generation sequencing (NGS), including metagenomic approaches, sequences fungal DNA directly from clinical samples, identifying rare or novel pathogens with broad-range primers and enabling detection in polymicrobial settings. Point-of-care tests, such as the T2 Magnetic Resonance system for Candida species, provide rapid (within hours) bloodstream detection without culture, improving outcomes in candidemia by facilitating early therapy. The 2025 British Society for Medical Mycology (BSMM) guidelines update strengthens recommendations for molecular assays like PCR for Pneumocystis jirovecii, Candida, and Mucorales, as well as 1,3-β-D-glucan testing for and *, and expands Aspergillus antigen/antibody testing to ICU and chronic respiratory disease patients, based on evidence accumulated since 2015. Emerging non-invasive imaging innovations include (PET) with radiotracers such as 68Ga-TAFC and 64Cu-JF5 for specific detection of invasive pulmonary , and MRI with CryptoCEST for identifying cryptococcal lesions via detection; these offer higher pathogen specificity than standard CT/MRI and are in early clinical evaluation or preclinical stages as of 2025. These innovations enhance accessibility and speed but require validation for routine use and cost reduction.

Differential diagnosis

Differentiating fungal infections from other conditions is crucial, as symptoms often overlap with bacterial, viral, parasitic, or non-infectious etiologies, potentially leading to delayed or inappropriate therapy. For superficial fungal infections like tinea (), common mimics include bacterial , which presents with pustules and responds to antibacterials; , characterized by silvery scales and nail pitting; and eczema, featuring pruritic, weeping lesions without annular borders typical of tinea. Key discriminators involve clinical morphology—such as central clearing in tinea versus uniform in —and lack of response to topical steroids or antibiotics. In subcutaneous infections, such as , differentials encompass bacterial abscesses, which form acute, tender fluctuant masses; cutaneous , presenting with verrucous or ulcerative nodules; and , featuring crusted ulcers often linked to exposure in endemic areas. Distinguishing features include the lymphocutaneous spread in versus localized suppuration in abscesses, and travel history aiding in ruling out . Systemic fungal infections pose broader challenges, mimicking (e.g., versus , both causing cavitary lesions and constitutional symptoms); viral infections like (CMV) , which may present with interstitial patterns; malignancies such as , forming mass-like opacities; and non-infectious conditions like , with granulomatous inflammation. For instance, often simulates in endemic regions, with miliary dissemination or mediastinal adenopathy. In , the CT halo sign—a nodule surrounded by —suggests angioinvasion but can overlap with bacterial septic emboli or Wegener's granulomatosis, necessitating correlation with or . Special considerations arise in post-COVID-19 , where secondary fungal infections like or mimic persistent bacterial or , exacerbated by use and . Clinicians must evaluate for risk factors like prolonged ICU stays to differentiate these from primary progression or superinfections. and remain essential to confirm fungal and avoid misdiagnosis, as histopathological examination reveals tissue and morphology, while identifies species, resolving ambiguities from imaging or alone. These methods complement diagnostic tests by providing definitive proof, particularly when empirical antibacterials fail.

Prevention

Prophylactic measures

Prophylactic measures for fungal infections primarily focus on personal , environmental precautions, and targeted interventions for vulnerable individuals to reduce exposure and susceptibility. These strategies are particularly emphasized for high-risk groups, such as immunocompromised patients, to prevent both superficial and invasive infections. By integrating daily habits and protective actions, individuals can significantly lower their risk of acquiring fungi from , water, or contaminated surfaces. Hygiene practices form the cornerstone of preventing superficial fungal infections, such as ringworm and . Maintaining clean, dry skin is essential, as moisture promotes fungal growth; regular washing and thorough drying, especially in , help mitigate this risk. Avoiding shared personal items like towels, combs, or clothing prevents direct transmission of dermatophytes. In healthcare settings, rigorous hand using alcohol-based sanitizers or soap and water is critical to curb the spread of opportunistic fungi like Candida auris. For foot-related infections, changing socks and shoes frequently and ensuring footwear allows air circulation further reduces moisture buildup. Protective gear is recommended for activities involving potential fungal exposure, particularly in occupational or recreational settings. Gardeners and those handling or materials should wear gloves to prevent subcutaneous infections like , often called "rose gardener's disease," caused by . In endemic areas for (Valley fever), such as the , N95 masks or respirators are advised during dusty conditions to avoid inhaling spores from . Long sleeves, pants, and closed-toe shoes provide additional barriers against cutaneous entry points. Lifestyle modifications play a key role in reducing susceptibility, especially for those with underlying conditions. Individuals with should maintain optimal blood glucose control, as impairs immune responses and increases vulnerability to infections like . Avoiding barefoot walking in public areas, such as locker rooms or pools, prevents acquisition of tinea pedis from contaminated floors. Adhering to prescribed medications and minimizing antibiotic use, which disrupts normal flora, also helps preserve natural defenses against opportunistic fungi. Vaccination options for fungal infections remain limited, with no approved vaccines currently available for human use against major pathogens. Experimental vaccines targeting Candida species and have shown promise in preclinical and early clinical studies, but none have progressed to widespread approval due to challenges in and safety. In June 2025, researchers at the reported preclinical success with the NXT-2 vaccine candidate, which protected against , Candida auris, and in mouse models, advancing toward potential human trials. Research continues to explore subunit and whole-organism approaches to elicit protective immunity. For high-risk patients, such as those undergoing or , antifungal prophylaxis is a standard clinical strategy. patients with anticipated profound and prolonged are recommended to receive oral triazoles like to prevent . In allogeneic recipients with (GVHD), prophylaxis is advised for those at high risk of invasive . These regimens are tailored based on local and patient-specific factors to balance efficacy and resistance risks.

Public health strategies

Public health strategies for controlling fungal infections emphasize coordinated , environmental interventions, institutional guidelines, educational efforts, and international collaborations to mitigate spread and resistance. systems play a critical role in monitoring fungal infections. The Centers for Disease Control and Prevention (CDC) has tracked Candida auris outbreaks in the United States since its first detection in 2016, with clinical cases rising from 53 in 2016 to 4,514 in 2023, enabling early detection and response to this multidrug-resistant pathogen. The World Health Organization (WHO) promotes antifungal stewardship programs as part of broader efforts, integrating fungal to optimize antifungal use and track emerging threats. Environmental controls target sources of fungal exposure in high-risk settings. In endemic areas for , such as the , measures recommend reducing construction-related dust through , water spraying, and limiting soil disturbance to prevent of spores. For species, which can proliferate in hospital water systems, routine protocols, including and disinfection, are implemented to limit contamination and reduce nosocomial transmission risks. Guidelines from professional societies guide institutional practices. The Infectious Diseases Society of America (IDSA) recommends high-efficiency particulate air () filtration in hospital rooms for high-risk patients, such as hematopoietic stem cell transplant recipients, to reduce airborne exposure and prevent invasive . Educational campaigns raise awareness to prevent infections and resistance. Public health initiatives highlight travel risks to histoplasmosis-endemic regions, such as the and valleys, advising avoidance of activities like cave exploration or soil disturbance that stir bat or bird droppings. Programs also educate healthcare providers and the public on judicious antifungal use to combat resistance, with resources from the CDC emphasizing recognition of resistant strains like Candida auris. Global initiatives coordinate responses to fungal threats. The WHO's 2022 Fungal Priority Pathogens List identifies 19 key fungi, categorized by threat level, to direct research funding, diagnostics development, and surveillance priorities, including critical pathogens like and Candida auris. In India, following the post-2020 COVID-19 surge in cases, the issued alerts in 2021 to enhance early detection and management in healthcare facilities.

Treatment

Antifungal therapies

Antifungal therapies primarily consist of pharmacological agents that target key components of fungal cell structure and function, with the main classes being polyenes, azoles, and echinocandins. Polyenes, such as , bind to in the fungal , forming pores that lead to ion leakage and cell death; this class is reserved for severe systemic infections due to its broad-spectrum activity and intravenous administration. Azoles, including , inhibit the enzyme 14-alpha-demethylase, disrupting biosynthesis and impairing membrane integrity; they are widely used for treating owing to their oral and favorable safety profile. Echinocandins, exemplified by , noncompetitively inhibit beta-1,3-glucan synthase, weakening the fungal and causing ; these agents are preferred for and , particularly in critically ill patients. Indications for these therapies vary by infection site and severity. Topical formulations of azoles, such as clotrimazole or miconazole, are first-line for superficial infections like and vulvovaginal , providing localized action with minimal systemic absorption. For life-threatening systemic infections, intravenous remains a cornerstone, particularly for , where lipid formulations are often employed to enhance tolerability while maintaining efficacy against Mucorales species. , such as paired with flucytosine, is standard for cryptococcal , as it accelerates fungal clearance and improves survival rates compared to monotherapy. Therapy selection may be guided by diagnostic susceptibility testing to optimize outcomes. Antifungal resistance poses a growing challenge, with mechanisms including efflux pumps that expel drugs from fungal cells, notably in azole-resistant Candida species where overexpression of ABC transporters like Cdr1p reduces intracellular drug accumulation. Point mutations in target enzymes, such as Erg11p for azoles, further diminish drug binding affinity. Globally, resistance among Candida bloodstream isolates has risen, with approximately 6% of U.S. surveillance samples showing resistance, and higher rates in emerging pathogens like Candida parapsilosis exceeding 10% in some regions. Pharmacokinetic considerations influence dosing and monitoring. , a broad-spectrum , undergoes hepatic metabolism primarily via , , and , leading to significant drug-drug interactions; for instance, coadministration with CYP inducers like rifampin can reduce levels by up to 80%, necessitating dose adjustments. Liposomal mitigates the associated with conventional formulations by altering tissue distribution, reducing the incidence of from over 50% to around 20% in clinical use. Recent advancements include rezafungin, a long-acting approved in 2023 for candidemia and in adults with limited alternatives; its once-weekly dosing stems from high and slow clearance, offering convenience over daily echinocandins like . Olorofim, an investigational orotomide that inhibits in the pyrimidine synthesis pathway, shows promise against resistant molds like and Lomentospora prolificans; a phase 2b trial published in 2025 demonstrated efficacy with a 51% partial or complete response rate at day 42 in patients with invasive fungal diseases and few treatment options, with phase 3 trials ongoing (estimated completion 2026) following FDA feedback on data in 2023.

Supportive and adjunctive treatments

Surgical interventions play a critical role in managing certain fungal infections by removing infected or necrotic tissue, thereby facilitating penetration and reducing fungal burden. In rhino-orbital , aggressive surgical of necrotic tissue is essential, often repeated as needed to control disease progression and improve survival rates when combined with therapy. For mycetoma, of localized lesions is indicated to decrease the microbial load and enhance response to medical treatment, though may be required in advanced cases. In fungal endocarditis, surgery is recommended for affected patients without contraindications, as it addresses the source of infection and prevents . Immune reconstitution strategies are vital for immunocompromised patients with fungal infections, aiming to restore host defenses. In patients, transfusions can bridge the period of severe , providing functional neutrophils to combat invasive fungal infections such as or , with evidence supporting their use in early intervention to improve outcomes. For transplant recipients, reducing therapy when feasible helps mitigate ongoing risk without precipitating graft rejection. In (CGD), where patients are prone to recurrent fungal infections, reducing immunosuppression supports immune recovery. Adjunctive therapies enhance antifungal efficacy by targeting host factors or fungal physiology. Hyperbaric oxygen therapy (HBOT) has been investigated as an adjunctive treatment for necrotizing fungal infections like , as elevated oxygen levels may exhibit fungistatic effects, inhibit fungal growth, and promote tissue healing, particularly in refractory cases; however, there is insufficient evidence to support its routine use. therapy, such as interferon-gamma (IFN-γ), is used in CGD to augment function and reduce the frequency of severe fungal infections, with long-term prophylaxis demonstrating tolerability and efficacy in lowering rates. Symptom management addresses the debilitating effects of fungal infections to improve quality of life. Analgesics, including antineuropathic agents, are administered for severe associated with invasive infections like rhino-orbital , which can cause trigeminal neuropathy requiring around-the-clock relief. Nutritional support is provided in disseminated disease to counteract in immunocompromised hosts, aiding overall recovery though specific protocols vary by status. Monitoring treatment response ensures optimal management and early detection of failure. (TDM) for azoles like and is recommended due to variable , guiding dose adjustments to achieve therapeutic levels and minimize toxicities such as QT prolongation. Serial imaging, including FDG-PET/CT, assesses lesion resolution and guides therapy modifications in invasive fungal diseases, often leading to changes in management in approximately half of cases.

Epidemiology

Global burden and distribution

Fungal infections impose a substantial burden, with recent estimates indicating approximately 6.5 million cases of invasive fungal infections annually, leading to about 3.8 million deaths worldwide, of which roughly 2.5 million are directly attributable to the infection. This figure represents a near doubling of mortality compared to earlier assessments, largely due to underdiagnosis in resource-limited settings where diagnostic tools are scarce. Superficial fungal infections, particularly dermatophytoses affecting the skin, , and , affect an estimated 1.73 billion people globally as of 2021, contributing to significant morbidity but lower mortality. Certain fungal infections exhibit distinct geographic distributions, with endemic mycoses concentrated in specific regions due to environmental factors like soil composition and climate. , caused by , is highly prevalent in the and valleys in the United States, as well as along the basin in . , or Valley fever, is primarily found in the arid , northern , and parts of Central and , with an estimated 350,000 annual cases in the U.S. alone. predominates in tropical regions of , particularly , , and , where it often manifests as a chronic pulmonary or mucocutaneous disease. Immunocompromised populations bear a disproportionate burden, with millions of individuals, particularly those with , cancer , or , experiencing severe fungal infections each year. These infections are particularly severe in low- and middle-income countries, where limited access to diagnostics and antifungals exacerbates outcomes; for instance, cases are overwhelmingly reported from , accounting for a substantial portion of global incidences due to high rates of uncontrolled and post-COVID-19 complications. Economically, fungal infections strain healthcare systems, with direct medical costs in the United States exceeding $13.4 billion annually as of 2025, including significant expenditures from hospitalizations for conditions like candidemia, which alone drives costs due to prolonged intensive care stays. Globally, the burden translates to billions in lost productivity, with higher impacts in low-income regions where 90% or more of severe cases like occur amid resource constraints. is driving the expansion of endemic ranges for certain fungal pathogens, altering their geographic distribution and increasing human exposure. For instance, , caused by the dimorphic fungus , is projected to extend northward into previously unaffected regions of the , including parts of , , and Washington, due to rising temperatures and shifting patterns. Models indicate that suitable climatic conditions for C. immitis and C. posadasii could lead to a 12% increase in cases over the next decade, with further expansion by 2030 as arid environments become more hospitable. In 2024, reported a record high of nearly 12,500 cases of Valley fever, underscoring the ongoing spread. Recent outbreaks highlight the rapid global dissemination of multidrug-resistant fungi. Candida auris, first identified in 2009, has caused hospital-associated clusters in over 40 countries across six continents, persisting on surfaces and evading standard disinfection protocols. In 2025, U.S. cases of C. auris nearly tripled, with over 2,800 diagnoses reported across more than 21 states, and outbreaks confirmed in additional European countries including , , and . Between 2020 and 2022, COVID-19-associated surged in , with over 45,000 cases reported, largely linked to use, , and disrupted healthcare during the . Antifungal resistance is escalating, complicating treatment and contributing to higher mortality. Echinocandin-resistant Candida species, particularly C. glabrata, have shown prevalence rising to 5-12% in intensive care units, driven by prior exposure to these first-line agents. Additionally, widespread agricultural use of azole fungicides has selected for environmental resistance in pathogens like , enabling cross-resistance to clinical azoles and increasing invasive risks. Novel threats underscore the evolving fungal landscape. Reports of Coccidioides emergence in the Pacific Northwest, including Washington state, signal potential establishment of new endemic foci beyond traditional southwestern boundaries. Post-flood events have also triggered aspergillosis surges, as seen after Hurricane Harvey in 2017, where damaged buildings fostered mold proliferation and invasive infections in vulnerable populations. In response, the has enhanced global surveillance through initiatives like the Fungal Priority Pathogens List and the GLASS-FUNGI module to track resistance and outbreaks. stewardship programs promote judicious use of therapies to preserve efficacy, emphasizing diagnostics and control in high-risk settings.

History

Early observations and discoveries

Fungal infections have been recognized in records for millennia, though early descriptions often conflated them with other ailments. Biblical accounts in the , particularly references to "leprous" conditions under the term tsaraath in Leviticus, likely encompassed a range of dermatological disorders, including possible fungal infections such as tinea, characterized by scaly, ring-like lesions. Similarly, Hippocratic writings around 400 BCE described oral ulcers known as aphthae, now interpreted as thrush or , marking one of the earliest documented fungal infections. The 19th century brought pivotal scientific advancements in identifying fungi as causative agents of human disease. In 1837, Polish-German physician and neurologist Robert Remak first observed fungal elements, including hyphae and arthroconidia, in crusts from patients with favus, a severe form of tinea capitis, establishing the parasitic nature of the infection. Building on this, Johann Lucas Schönlein, a prominent German clinician, announced in 1839 the fungal etiology of favus during a lecture and named the organism Achorion schönleinii (later reclassified as Trichophyton schoenleinii), representing the first clear attribution of a human disease to a fungal pathogen. Microscopic examinations around this period, including those by contemporaries like David Gruby, further confirmed the presence of mycelial structures in skin scrapings from ringworm cases, shifting perceptions from mere superstition to empirical observation. Early subcutaneous fungal infections also emerged in descriptions from the . In 1892, Argentine medical student Alejandro Posadas reported the first case of what is now known as in a soldier from , initially mistaking the spherule-filled lesions for a protozoal infection resembling ; this endemic mycosis, caused by species, highlighted regional variations in fungal . Similarly, , a chronic dematiaceous fungal infection, was first detailed in 1914 by German physician Max Rudolph in rural , though retrospective analyses suggest earlier unrecognized cases may date to the late among agricultural workers exposed to soil trauma. Prior to the formalization of in , many fungal infections were misattributed to bacterial contamination, parasitic worms, or even , delaying acceptance of fungi as primary pathogens. Investigators often viewed observed mycelia as secondary invaders rather than etiological agents, a misconception rooted in limited and the prevailing of disease. These early hurdles underscored the need for rigorous isolation and experiments to validate fungal causality.

20th-21st century developments

In the early 20th century, significant microbiological advances illuminated the nature of fungal pathogens. In 1906, Samuel Taylor Darling identified during an in , marking the first description of this responsible for , initially mistaken for a . The 1940s brought recognition of thermal dimorphism in pathogenic fungi, with researchers like Arthur Henrici noting that species such as and switch between yeast and mold forms in response to temperature, a trait central to their virulence and tissue invasion. By the 1980s, the epidemic drove a surge in opportunistic fungal infections, particularly caused by , which emerged as a leading cause of in immunocompromised patients, with incidence rising dramatically due to cell depletion. Therapeutic progress transformed management of fungal infections from the mid-20th century onward. , a polyene , was introduced in 1958 as the first effective systemic agent against deep-seated mycoses, binding to in fungal membranes to disrupt cell integrity, though its limited use. The 1990s saw the advent of azole antifungals, including approved in 1990, which inhibits synthesis via enzymes, offering oral bioavailability and reduced toxicity for prophylaxis and treatment of and in AIDS patients. In the , echinocandins like (approved 2001) provided a new class targeting β-1,3-glucan synthesis in the fungal , proving effective against and with a favorable safety profile. Epidemiological patterns shifted markedly, influenced by global health crises. During the 2003 SARS outbreak, corticosteroid therapy in critically ill patients led to cases of invasive pulmonary aspergillosis, highlighting secondary fungal superinfections in viral pandemics. The from 2020 amplified incidence, particularly in and among diabetics, with and immune dysregulation contributing to over 40,000 cases and high mortality rates exceeding 50%. Updated estimates from 2024 indicate a higher global burden, with 6.5 million invasive fungal infections annually and 3.8 million deaths, of which about 2.5 million are directly attributable to fungal diseases, underscoring their underrecognized burden comparable to or . Diagnostic innovations enhanced early detection. In the 1970s, detection assays emerged, such as the latex agglutination test for cryptococcal capsular , enabling rapid serum and cerebrospinal fluid diagnosis with sensitivity over 90% in AIDS-related cases. The introduced next-generation sequencing (NGS) for unbiased identification, allowing metagenomic of clinical samples to detect rare or mixed fungal infections, with applications in immunocompromised patients improving diagnostic yield by identifying species missed by culture. Policy responses addressed rising antifungal resistance and surveillance gaps. In 2022, the released its first Fungal Priority Pathogens List, categorizing 19 fungi into critical, high, and medium priority groups to guide , diagnostics, and for threats like azole-resistant . In April 2025, the WHO published its first-ever reports on tests and treatments for fungal infections, addressing the critical lack of medicines and diagnostic tools for invasive fungal diseases. This initiative spurred global action plans, emphasizing laboratory , programs, and international collaboration to mitigate resistance, similar to bacterial AMR strategies.

Fungal infections in other organisms

Infections in animals

Fungal infections are prevalent in non-human animals, particularly mammals, and pose significant challenges in due to their potential for systemic spread and economic repercussions in and conservation. These infections often mirror those in humans in terms of causative agents and clinical manifestations, though animal hosts exhibit species-specific susceptibilities influenced by environmental exposure and immune status. Common examples include , which affects the respiratory system in dogs and birds, caused by and leading to nasal discharge, coughing, and in severe cases, dissemination to other organs. , primarily involving or C. gattii, is the most frequent systemic mycosis in cats, often presenting as chronic , skin lesions, or neurological signs following inhalation of environmental spores. , commonly known as ringworm, impacts livestock such as and sheep, manifesting as circular alopecia and crusty lesions on the skin and , typically due to Trichophyton verrucosum or species. Several fungal infections in animals carry zoonotic potential, facilitating transmission to humans through direct contact or environmental contamination. , a primary cause of ringworm in dogs and cats, readily spreads to humans via pet handling, accounting for a notable proportion of zoonotic dermatophytoses in household settings. Similarly, , induced by , infects various mammals through inhalation of spores from soil enriched with bat guano, with outbreaks linked to exposure in endemic regions affecting both and domestic animals. Veterinary-specific examples highlight regional and ecological variations in disease prevalence. , caused by the —a fungal-like —predominantly strikes horses in tropical and subtropical areas, resulting in cutaneous or gastrointestinal lesions from contact with contaminated water sources. In dogs, due to is endemic to the Ohio and valleys , causing pulmonary, cutaneous, or multi-organ involvement with symptoms like , lameness, and ocular . Diagnosis and treatment of fungal infections in animals parallel approaches but face unique hurdles, especially in non-domestic . Veterinary diagnostics rely on cytology, culture, , and , while treatments often employ antifungals like , which is effective against systemic mycoses in dogs and cats, administered orally for months to achieve resolution. In , challenges include limited access for sampling, delayed presentation of symptoms, and difficulties in monitoring therapy, complicating efforts to curb outbreaks in free-ranging populations. Fungal infections exact a heavy economic toll on and threaten conservation. In , caused by Candida contributes to mortality in farmed under stress, exacerbating losses that rank fungal diseases second only to bacterial infections and contributing to overall disease-related losses estimated at $6 billion annually in reduced yields and treatment. For , ringworm impairs and hide quality, leading to substantial productivity declines in herds. Conservation efforts are undermined by , driven by , which has precipitated global amphibian declines; a 2019 assessment linked the pathogen to the loss of at least 501 , including 90 presumed extinctions, underscoring its role in crises.

Infections in plants

Fungal infections pose a significant threat to plant health, particularly in and , where they can devastate crops and ecosystems. These pathogens, primarily from the and phyla, infect a wide range of , leading to reduced yields, quality degradation, and contributing to economic losses from plant pests and diseases estimated at over $220 billion annually worldwide. Unlike bacterial or viral infections, fungal diseases often involve complex life cycles that enable rapid spread and persistence in the environment. Major plant pathogens include rust fungi such as species, which cause rusts by forming pustules on leaves and stems, disrupting and weakening plants. Smut fungi like species infect grasses and , replacing plant tissues with spore-filled that render crops inedible. Powdery mildews, caused by Erysiphe species, produce white fungal growth on leaf surfaces, impairing and leading to premature defoliation. Fusarium wilt agents, including strains, colonize vascular tissues, blocking water transport and causing wilting in crops like tomatoes and bananas. Notable disease examples illustrate the severity of these infections. , caused by the ascomycete Ophiostoma novo-ulmi and related species, spreads through elm bark beetles, leading to vascular blockage and tree death; it has eliminated millions of trees in and since the . Rice blast, induced by Magnaporthe oryzae, results in lesions on rice leaves and panicles, contributing to annual global losses exceeding $60 billion and threatening in . Transmission of these fungal infections typically occurs via airborne spores dispersed by wind, soilborne propagules that persist for years, or vectors like insects that carry inoculum between plants. Many pathogens exhibit polycyclic life cycles, with multiple infection rounds per season, and some require alternate hosts—such as barberry for wheat stem rust (Puccinia graminis)—to complete sexual reproduction and generate genetic diversity. The impacts extend beyond plants to human concerns, primarily through threats to food security and health risks from mycotoxins. The 2010 outbreak of wheat stem rust race UG99 (Puccinia graminis f. sp. tritici) in East Africa and the Middle East affected over 80% of global wheat varieties, prompting international efforts to develop resistant strains and avert famine. Additionally, fungi like Aspergillus species produce aflatoxins in contaminated crops such as maize and peanuts, which are potent carcinogens linked to liver cancer and immune suppression in humans upon consumption. Some genera, such as Fusarium, cause infections in both plants and humans, highlighting shared vulnerabilities. Management strategies focus on integrated approaches, including the application of fungicides like triazoles and strobilurins to suppress , though resistance is emerging similarly to patterns observed in human therapies. Breeding resistant varieties, such as those with R-genes that trigger hypersensitive responses to pathogens, has been pivotal; for instance, pyramiding multiple resistance genes in combats Magnaporthe oryzae evolution. Cultural practices, including and sanitation to reduce inoculum, complement these efforts, emphasizing prevention over cure in .

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