Classification & Types

Introduction/Definitions:

Fungi are eucaryotes that has ergosterol as a key component rather than cholesterol. This is an importance difference since many antifungal agents are directed towards ergosterol. Fungi also have a rigid cell wall that contains chitin as well as hyphae which are branching, threadlike tubular filaments.

Most fungi are not pathogens but they can produce toxins and cause allergies (primarily ). For example, spoiled peanuts and other grains contain coumarin derivatives produced by Aspergillus flavus and cause liver damage. Claviceps purpura also infects grains and produces lysergic acid diethylamide, commonly known as “LSD”.

The phylum Ascomycota contains about 30k species and includes about 75% of the known fungi. Among the ascomycetes are important fungi such as bread yeasts. The ability of yeasts to fermetn carbohydrates, breaking down glucose to produce thanol and CO2, is exploited in the production of bread, beer, and wine. Penicillium chrysogenium produces penicillin.

Mycology is the study of fungi. The term for a fungal infection is mycosis.

The CCD identifies 3 types of fungal disease in humans: (1) community acquired infections in the general population caused by environmental pathogens, (2) hospital associated infections caused by fungal pathogens in clinical settings and (3) opportunistic infections caused by low virulence speciesinfecting already weakened individuals.

Fungi can cause health issues in humans by acting as allergens that trigger immune responses or by direct infection, usually of the skin or nails, or by producing toxins that are ingested.

Fungi are informally divided into unicellular yeasts and filamentous molds based on their overall appearance. Fungi are also sometimes classified as follows:

Superficial Mycoses 

Superficial mycoses live on dead skin and hair and do not elicit an immune response. Superficial mycoses include Tinea versicolr, Tinea nigra, Black and White piedra which grow on hair shafts.

cutaneous mycoses 

Cutaneous mycoses are caused by dermatophytes and infect keratinized skin, hair and nails. Cutaneous mycoses invoke an immune response. Diseases are very common and include ringworm or tinea (e.g., Tinea pedis).

–Dermatophytosis, (also called ringworm or tinea): see Superficial fungi infections

Dermatophytes are fungi that require keratin for growth. These fungi can cause superficial infections of the skin, hair, and nails. Dermatophytes are spread by direct contact from other people (anthropophilic organisms), animals (zoophilic organisms), and soil (geophilic organisms), as well as indirectly from fomites.

Potassium hydroxide (KOH) microscopy aids in visualizing hyphae and confirming the diagnosis of dermatophyte infection. Other diagnostic modalities include Wood’s lamp examination, fungal culture, and skin or nail biopsy. See Hainer (good discussion)

Tinea is a common superficial fungal skin infection most often caused by Trichophyton, Microsporum, or Epidermophyton fungi and often treated using over-the-counter topical antifungal agents.

Tinea is a very common fungal infection of the skin. It is often called “ringworm” because the rash is circular, with a ring-like appearance.

Tinea infection can be diagnosed using fungal microscopy and culture, which allows for fungal speciation and viability assessment. Fungal microscopy of skin scrapings and nail clippings is performed on KOH (potassium hydroxide) and can be rapid.

Oral terbinafine is a first-line antifungal treatment for extensive skin infections, which typically occur in immunocompromised or older persons. Outbreaks of extensive, recalcitrant, and frequently terbinafine-resistant dermatophytosis in immunocompetent persons are ongoing in southern Asia because of the recently emerged dermatophyte Trichophyton indotineae (formerly Trichophyton mentagrophytes genotype VIII). T. indotineae typically causes tinea faciei, corporis, or cruris; easily spreads person-to-person; and has been reported globally, including in multiple US states. Laboratory identification requires advanced molecular techniques because culture-based methods cannot distinguish T. indotineae from other Trichophyton species. There is an emergence of antifungal-resistant T. indotineae as a cause of genital lesions and possible acquisition and transmission through sexual contact. Clinicians should be aware that visual inspection without diagnostic testing cannot reliably distinguish dermatophytosis from other causes of inflammatory skin conditions (e.g., contact dermatitis). Spivack “Potential Sexual Transmission of Antifungal-Resistant Trichophyton indotineae”

—-Tinea pdeis (foot) causes itching, scaling, flaking and sometimes blistering of the affected areas. Tinea pedis are fungi that are typically transmitted in moist communal areas where people go barefoot, such as around swimming pools or in showers and require a warm moist environment like the inside of a shoe to incubate.

Exposure to occlusive footwear, sweating and communal spaces are predisposing factors of tinea pedis.6 The interdigital subtype is the most common form of tinea pedis, which manifests as maceration or scales between toes.

—-Tinea capitis is a dermatophyte infection of the scalp and hair and it predominantly occurs in pre-pubertal children

—-Tinea cruris (groin) also known as “crotch itch” or “jock itch” is a dermatophyte fungal infection of the groin region.

—-Tinea corporis (ringworm -body) is a superficial fungal infection of the arms and legs, especially on glabrous skin. However it may occur on any part of the body. It presents as a annual, marginated plaque with thin scale and clear center.

Tinea corporis, or ringworm, typically appears as single or multiple, annular, scaly lesions with central clearing, a slightly elevated, reddened edge, and sharp margination (abrupt transition from abnormal to normal skin) on the trunk, extremities, or face.

Treatment includes grisofluvine, itraconazole and clotrimazole cream. Treatment typically includes measures to decrease excessive skin moisture and the use of topical antifungal creams.

—-Trichophyton rubrum (T. rubrum) is a dermatophyte responsible for causing the majority of superficial fungal infections worldwide. Dermatophytes are a subset of fungi that have the ability to invade keratinized tissues, such as skin, hair, and nails. This group of fungi can cause infection anywhere on the skin, however, they most commonly affect the feet, inguinal region, axillae, scalp, and nails. The infection results in mild to moderate dermatological symptoms, with a range of severity of infection. Such variations are believed to be a result of the host’s immune response to the microorganism. This response is elicited by the keratinocytes, which are the first line of defense against microorganisms, such as T. rubrum. Several Toll-like receptors, such as TLR2, TLR4, TLR6, and Human Beta Defensin (HBD)-1, HBD-2, IL-1B, and IL-8, are expressed as part of the initial host defense. See Blutfield

—-Tinea versicolor is caused by Malassezia species, notably M. globosa, M. furfur and M. sympodialis. The condition is characterized by scaly hypopigmented or hyperpigmented macules/patches, primarily located on the upper trunk, neck and upper arms. The diagnosis is usually based on characteristic clinical features. If necessary, a potassium hydroxide preparation test can be performed to reveal numerous short, stubby hyphae intermixed with clusters of spores. Most patients with tinea versicolor respond to topical antifungal therapy, which has a better safety profile (fewer adverse events, fewer drug interactions) and lower cost compared to systemic treatment and is therefore the treatment of choice. Oral antifungal therapy is typically reserved for patients with extensive disease, frequent recurrences or disease that is refractory to topical therapy. Advantages of oral antifungal therapy include increased patient compliance, shorter duration of treatment, increased convenience, less time involved with therapy and reduced recurrence rates. On the other hand, oral antifungal therapy is associated with higher cost, greater adverse events and potential drug–drug interactions and is therefore not the first-line treatment for tinea versicolor.

—-Tinea unguium, also known as onychomycosis, is a dermatophyte infection of the nails. Onychomycosis is very common in the elderly with a prevalence of up to 50% in people aged over 70 years. Nearly half of patients with toenail onychomycosis were found to have concomitant fungal skin infections, most commonly tinea pedis

Ketoconazole is a synthetic imidazole antifungal drug that is used to treat fungal infections such as tinea.

—-Tinea gladiatorum (TG; trichophytosis gladiatorum; tinea gladiatorum) is the most widespread fungal skin infection among contact sports athletes and the second most common skin infection in this group in general, after herpes gladiatorum (HSV infection). T. tonsurans is a microorganism of a filamentous fungi group, dermatophytes (subdivided into seven genera: Trichophyton, Microsporum, Epidermophyton, Paraphyton, Lophophyton, Arthroderma, and Nannizzia), which are keratinophilic and keratinolytic pathogens.

subcutaneous mycoses 

Subcutaneous mycoses are lesions in deeper skin layers usually caused by a trauma such as a thorn. For example,  sporotrichosis (“Rose grower’s disease”) typically occurs when one is pricked by a thorn which has the Sporothrix schenckii fungus agent. Other subcutaneous infections are Chromoblastomycosis and Mycetoma.

Sporotrichosis (Sporothrix brasiliensis): Sporothrix brasiliensis is considered a highly virulent emerging pathogen that casues sporotrichosis in humans, mainly after zoonotic transmission from infected cats. Iis an implantation mycosis caused by fungi in the genus Sporothrix. It affects humans and other mammals. Sporotrichosis is a globally neglected epizoonotic and sapronotic disease, primarily affecting the skin and subcutaneous tissues, cuased by fungi of the Sporothrix genus, and represents the most prevalent implantation mycosis in Latin American, expecially in Brazil. Sporothris spp. are thermally dimorphic fungi showing filamentous forms at 25-30C and yeast like forms at 35-37C, as in mammals. The main clinical pathogenic species are S. brasiliensis, S. schenckii, S. globesa and S. lurici.  (Prado, “Sporothrix brasiliensis treatment failure without initial elevated itraconazole MICs in felids at border of Brazil” Emerging Infectious Disases, 2025).

Cat-transmitted sporotrichosis caused by Sporothrix brasiliensis is an emerging zoonosis in Latin America. Although cat-transmitted sporotrichosis casued by the highly transmissible Sporothrix brasiliensis species is an increasing concern in Latin America, S. Brasiliensis has not been detect in the US and cat-transmitted Sporothrix schenckii is rarely reproted. However recently a clustor of sporotrichosis cases involving 2 domestic cats and zoonotic transmission between one of the affected cats and a veterinary technician was reported. (Toda “Sporotrichosis Cluster in domestic cats and veterinary technician, Kansas, USA, 2022” Emergingin Infectious Diseases, May 2024).

Early diagnosis of sporotrichosis and early treatment initiation with appropirate antifungal drugs can improve outcomes and help prevent transmission to other cats or humans. Cytology and culture should be considered for wounds or lesions taht fail to respond to antibiotics. Itroconazole should be given to cats with food to improve adsorption, and potassium iodide in combination with itraconazole can improve treatment of efficacy in cats with multiple or extensive lesions or in treatment refractory cases. (Toda “Sporotrichosis Cluster in domestic cats and veterinary technician, Kansas, USA, 2022” Emergingin Infectious Diseases, May 2024).

To reduce zoonotic transmission risk, veterinary professionals should wear examination gloves when handling cats with suspected sporotrichosis and take precautions to avoid scratches or bits. Wounds form scratches or bits should be washed promptly with soap and water. (Toda “Sporotrichosis Cluster in domestic cats and veterinary technician, Kansas, USA, 2022” Emergingin Infectious Diseases, May 2024).

The drug of choice is itraconaole. Cats should receive itraconazole (25-100 mg/d) and those with disseminated and exztracutaneous forms potassium iodid (25-20 mg/kg/24h, depending on the severity of symptoms).

systemic mycoses 

Systemic mycoses are inheritently infectious and include (1) Histoplasmosis otherwise known as “Darling’s” “cave” or “spelunker’s” disease. Histoplasmosis occurs in the midwest. Infection is due to inhalation of conidia or hyphal fragments which are phagocytized by pulmonary macrophages. It is usually found on bird dropping and is a dimorphic fungus in that it can exist in the yeast (e.g., macophages) or mold (e.g., soil) form. Treatment may include itraconazole and/or amphotericin B. (2) Blastomycosis otherwise known as “Gilchrist’s” or “Chicago” disease is endemic in Ohio and the Mississippi Valley. Treatment can again be amphotericin B. (3) Coccidioidomycosis otherwise known as “Posada-Wernicke” or “San Joaquin Valley vever” is endemic in California and Texas. Treatment can again include amphotericin

Histoplasmosis: see CDC (good description) CDC (prevention)

Histoplasmosis otherwise known as “Darling’s” “cave” or “spelunker’s” disease. Histoplasmosis occurs in the midwest. Infection is due to inhalation of conidia or hyphal fragments which are phagocytized by pulmonary macrophages. It is usually found on bird dropping and is a dimorphic fungus in that it can exist in the yeast (e.g., macophages)  or mold (e.g., soil) form. Treatment may include itraconazole and/or amphotericin B.

The etiologic agent of histoplasmosis, Histoplasma, is a cosmopolitan fungus detected in all continents, including Antartica. Histoplasmin, the main Histoplasma antigen, skin testing has revealed the fungus has a large geographic range. Nuclear gene geneologies and a global sample of Histoplasma strains from 8 countries revealed the existence of more than 7 phylogenetic species, monophyletic groups that are reciprocally monophyletic and isolated from each other. (Matute, “High genetic diversity of Histoplasma in the Amazon Basis, 2006-2017” Emerging Infectious Diseases, 31(6), 2025).

Histoplasmosis is common in the Mississippi and Ohil Valleys in the US and the disseminated form was calssified as an AIDS definicning disease in 1987.

Considering fungal growth patterns, it can take more than 2 weeks to observe mycelial growth, which can significantly delay diagnosis. Positive cultures are more likely to be found in disseminated disease due to the presumed higher fungal burden in the host. When histopathology is available, finding yeast cells in tissue is consistent with Histoplasma and supports the diagnosis. Another important diagnostic method is antigen detection. Antigen testing (i.e. detection of Histoplasma polysaccharide by antibodies) can be done on any body fluids and tissues depending on the suspected site of infection but is most often tested in the urine.

Histoplasma is a dimorphic fungus that grows as a mold in the environment and as a yeast in human tissues. Human histoplasmosis is caused by two distinct organisms: Histoplasma capsulatum var. capsulatum and Histoplasma capsulatum var. duboisii. While H. capsulatum var. duboisii occurs exclusively in Africa, H. capsulatum var. capsulatum has been identified on all continents except for Antarctica.

–Histoplasma capsulatum: causes respiratory and disseminated disease, even in immunocompetent hosts. In contrast to opportunistic pathogens, which are readily controlled by phagocytic cells, H. capsulatum yeasts are able to infect macrophages, survive antimicrobial defenses, and proliferate as an intracellular pathogen. In the environment, H. capsulatum grows as a saprobic conidia-producing mycelium. When H. capsulatum-contaminated soil is disturbed, the aerosolized mycelium fragments and conidia may be inhaled, and the small size of the conidia enables them to reach the lower respiratory track. H. capsulatum cells respond to the elevated temperature in the mammalian host by activation of a transcriptional program that induces a switch to the yeast-phase morphology and expression of factors required for pathogenesis. Factors produced by H. capsulatum yeast cells enable them to parasitize phagocytic immune cells. Pathogenic-phase yeasts are capable of invading phagocytic cells, including alveolar macrophages, polymorphonuclear leukocytes and dendritic cells. See Garfoot

H. capsulatum may be found in microfoci within endemic areas. These microfoci include soil enriched in nitrogen with pH levels between 5 and 10, which is usually due to large amounts of bird excreta or bat guano. The mycelial phase in the environment has two types of conidia: macroconidia measuring 8–14 µm in diameter with distinct tuberculate projections on the surface (ship’s wheel) and microconidia measuring 2–5 µm in diameter (infectious form). Microconidia formed in the mold phase can easily be aerosolized by disruption of their microfoci by farming, remodeling or demolition of old buildings, clearing areas where blackbirds have roosted, or exposure to chicken coops and caves. learing areas where blackbirds have roosted, or exposure to chicken coops and caves [1]. Infection occurs following the inhalation of microconidia, which can reach the lower respiratory tract. The temperature shift and changes in nutritional composition trigger the morphological transformation into yeasts. See Hague

The diagnosis of histoplasmosis can be ascertained by the direct observation or isolation of the pathogen (culture, histopathology, and cytopathology) or by the detection of antigens, antibodies, or nucleic acids. Clinical samples sent to the laboratory for culture are plated on a nutrient-poor medium such as Sabouraud agar and incubated at 25 ◦C to 30 ◦C. Mycelial growth occurs within 2 to 3 weeks but may take up to 8 weeks. The detection of H. capsulatum polysaccharide in urine and serum was first developed in 1986 as a sandwich radioimmunoassay and was subsequently reformulated into an enzyme immunoassay (EIA) in 1989. A second-generation EIA was introduced in 2004, which allowed for semiquantitative results and reduced the number of false-positive results caused by human antirabbit antibodies, and most recently, a third-generation quantitative test (MiraVista H. capsulatum Galactomannan EIA) was FDA-approved. Detection of anti-H. capsulatum-specific antibodies can aid in the diagnosis of certain histoplasmosis syndromes where antigen is unlikely to be positive (e.g., mediastinal granuloma, fibrosis) or increase the sensitivity in conjunction with antigen detection. Major pitfalls include the time required for antibody production following an infection (4–8 weeks) and the inability of certain immunocompromised patients to mount a detectable humoral response. The 3 most common antibody testing assays include complement fixation (CF), immunodiffusion (ID), and EIA. A CF titer of 1:8 or higher is found in most patients with histoplasmosis, though titers of >1:32 or higher more strongly suggest active infections. In addition, an acute infection can be diagnosed by a ≥4-fold rise in antibody titers taken at least 2 weeks apart. Molecular-based diagnostics rely on the detection of nucleic acid from a specific pathogen. There are a wide variety of laboratory-based polymerase chain reactions (PCR), though none are FDA-approved for clinical samples. The overall sensitivity of these tests ranges from 67% to 100%. See Hage

Blastomycosis otherwise known as “Gilchrist’s” or “Chicago” disease is endemic in Ohio and the Mississippi Valley.

Treatment can again be amphotericin B.

Coccidioidomycosis otherwise known as “Posada-Wernicke” or “San Joaquin Valley vever” is endemic in California and Texas.

Treatment can again include amphotericin B.

opportunistic mycoses 

B. opportunistic mycoses are pathogenic in immunocompetent individuals and include the following:

(1) Aspergillus:  Videos: Aspergillus (generally description) Aspergillus (danger noted)

Aspergillus spp. is a genus of saprophytic fungi, which is widely distributed in nature. This genus plays an important role in environmental nitrogen and carbon recycling and relies on conidia to spread in the air (Krüger et al. 2015; Latgé and Chamilos 2019). Among the approximately 200 Aspergillus species, less than 20 are pathogenic for humans (Paulussen et al. 2017; Mead et al. 2019). Aspergillus fumigatus exerts a major influence on the number of pathogenic Aspergillus strains.

Aspergillosis such as A. fumigatus, A. flavus, A. niger are ubiquitous in damp basements and vegetation. It can cause blockage of airways from fungal masses. Treatment can include surgery, amphotericin B or itraconazole. (2) Cryptococcosis neoformans (3) Candidiasis is a dimorphic fungus with yeast on mucosal surfaces. It is actually part of one’s normal flora in skin, mouth and intestines and stays as yeast but it forms hyphae when invasive. Treatment includes cessation of antibiotic and can also include itraconzaole.

Most fungi are not pathogens but they can produce toxins and cause allergies (primarily IgE mediated). For example, spoiled peanuts and other grains contain coumarin derivatives produced by Aspergillus flavus and cause liver damage. Claviceps purpura also infects grains and produces lysergic acid diethylamide, commonly known as “LSD”.

Aspergillosis such as A. fumigatus, A. flavus, A. niger are ubiquitous in damp basements and vegetation. It can cause blockage of airways from fungal masses.

Treatment can include surgery, amphotericin B or itraconazole.

–Aspergillus fumigatus: which most people inhale every day, can cause disease of the lungs but can also colonize other parts of the body including the brain, infectious-disease experts said. Hospitalizations related to severe Aspergillus infectionss are increasing.

Aspergillus fumigatus is one of the ubiquitous fungi with airborne conidia, which accounts for most aspergillosis cases. In immunocompetent hosts, the inhaled conidia are rapidly eliminated. However, immunocompromised or immunodeficient hosts are particularly vulnerable to most Aspergillus infections and invasive aspergillosis (IA), with mortality from 50% to 95%. Despite the improvement of antifungal drugs over the last few decades, the therapeutic effect for IA patients is still limited and does not provide significant survival benefits. The drawbacks of antifungal drugs such as side effects, antifungal drug resistance, and the high cost of antifungal drugs highlight the importance of finding novel therapeutic and preventive approaches to fight against IA.

It is estimated that humans may inhale as many as hundreds of A. fumigatus conidia every day (Alanio et al. 2017; Takazono and Izumikawa 2018). In healthy hosts, the inhaled conidia are rapidly eliminated by a competent immune system composed of innate and adaptive immunity. The innate immunity plays pivotal role in destroying most of the inhaled conidia in the respiratory tract by respiratory ciliary movement and proteins on the surface of epithelial cells, and in recognizing and engulfing the remaining conidia by alveolar phagocytes through surface pattern recognition receptors. Simultaneously, phagocytes also induce inflammatory chemokines and cytokines and recruit other immune cells to destroy surviving A. fumigatus spores and hyphae. Among them, neutrophils can prevent the formation of hyphae and kill it.

–Aspergillus flavus: In certain locales and hospitals, Aspergillus flavus is more common in air than A. fumigatus, for unclear reasons. After A. fumigatus, A. flavus is the second leading cause of invasive aspergillosis and it is the most common cause of superficial infection. Experimental invasive infections in mice show A. flavus to be 100-fold more virulent than A. fumigatus in terms of inoculum required. Particularly common clinical syndromes associated with A. flavus include chronic granulomatous sinusitis, keratitis, cutaneous aspergillosis, wound infections and osteomyelitis following trauma and inoculation. Outbreaks associated with A. flavus appear to be associated with single or closely related strains, in contrast to those associated with A. fumigatus. In addition, A. flavus produces aflatoxins, the most toxic and potent hepatocarcinogenic natural compounds ever characterized. Accurate species identification within Aspergillus flavus complex remains difficult due to overlapping morphological and biochemical characteristics, and much taxonomic and population genetics work is necessary to better understand the species and related species. The flavus complex currently includes 23 species or varieties, including two sexual species, Petromyces alliaceus and P. albertensis.

Like other Aspergillus species, A. flavus has a worldwide distribution. This probably results from the production of numerous airborne conidia, which easily disperse by air movements and possibly by insects. Atmosphere composition has a great impact on mould growth, with humidity being the most important variable. A. flavus appears to spend most of its life growing as a saprophyte in the soil, where it plays an important role as nutrient recycler, supported by plant and animal debris.

Cryptococcosis neoformans

Candidiasis: (see outline)

Trichosporonosis:

–Trichosporon asahii: is an emerging yeast-like fungal pathogen causing life-threatening catheter-related infections worldwide. Despite being often overlooked, the occurrence of invasive trichosporonosis has dramatically increased in reent decades, and crude mortality rates have reached up to 80%, depending on patients’ underlying conditions. Episodes of invasive trichosporonosis caused by T. asahii are primarily reported in long-term hospitalized patients with underlying hematologic malignancies and neutropenia, as well as among critically ill patients who have undergone invasive medical procedures. (Hagen, “Detection of multiple nosocomial Trichosporon asahii transmission events via microsatellite typing assay, South America”, Emerging Infectious Diseases (September 2025)

Triazoles, particularly voriconaole, are recommended as first line therapy for treating invasive trichosporonosis.