Systemic mycoses due to opportunistic pathogens are infections of patients 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.

Systemic mycoses due to primary pathogens originate primarily in the lungs and may spread to many organ systems. Organisms that cause systemic mycoses are inherently virulent. In general primary pathogens that cause systemic mycoses are dimorphic.

A 2003 survey of diseases of the foot in 16 European countries found onychomycosis to be the most frequent fungal foot infection and estimates its prevalence at 27%. Prevalence was observed to increase with age. In Canada, the prevalence was estimated to be 6.48%. Onychomycosis affects approximately one-third of diabetics and is 56% more frequent in people suffering from psoriasis.

No preventive measure is known aside from avoiding the traumatic inoculation of fungi. At least one study found a correlation between walking barefoot in endemic areas and occurrence of chromoblastomycosis on the foot.

Following effective treatment recurrence is common (10–50%).

Nail fungus can be painful and cause permanent damage to nails. It may lead to other serious infections if the immune system is suppressed due to medication, diabetes or other conditions. The risk is most serious for people with diabetes and with immune systems weakened by leukemia or AIDS, or medication after organ transplant. Diabetics have vascular and nerve impairment, and are at risk of cellulitis, a potentially serious bacterial infection; any relatively minor injury to feet, including a nail fungal infection, can lead to more serious complications. Infection of the bone is another rare complication.

The exact cause of Majocchi's granuloma is not well established however a dysfunctinoal immune system may be a causative factor. The first form of MG, the superficial perifollicular form occurs predominately on the legs of otherwise healthy young women who repeatedly shave their legs and develop hair follicle occlusions that directly or indirectly disrupt the follicle and allow for passive introduction of the organism into the dermis. Hence, the physical barrier of the skin is important because it prevents the penetration of microorganisms. Physical factors that play a major role in inhibiting dermal invasion include the interaction among keratin production, the rate of epidermal turnover, the degree of hydration and lipid composition of the stratum corneum, CO levels, and the presence or absence of hair. Keratin and/or necrotic material can also be introduced into the dermis with an infectious organism to further enhance the problem. In immunocompromised individuals, the use of topical corticosteroids may lead to a dermatophyte infection due to local immunosuppression.

Chromoblastomycosis occurs around the world, but is most common in rural areas between approximately 30°N and 30°S latitude. Madagascar and Japan have the highest incidence. Over two-thirds of patients are male, and usually between the ages of 30 and 50. A correlation with HLA-A29 suggests genetic factors may play a role, as well.

Tinea corporis is caused by a tiny fungus known as dermatophyte. These tiny organisms normally live on the superficial skin surface, and when the opportunity is right, they can induce a rash or infection.

The disease can also be acquired by person-to-person transfer usually via direct skin contact with an infected individual. Animal-to-human transmission is also common. Ringworm commonly occurs on pets (dogs, cats) and the fungus can be acquired while petting or grooming an animal. Ringworm can also be acquired from other animals such as horses, pigs, ferrets and cows. The fungus can also be spread by touching inanimate objects like personal care products, bed linen, combs, athletic gear, or hair brushes contaminated by an affected person.

Individuals at high risk of acquiring ringworm include those who:

- Live in crowded, humid conditions.

- Sweat excessively, as sweat can produce a humid wet environment where the pathogenic fungi can thrive. This is most common in the armpits, groin creases and skin folds of the abdomen.

- Participate in close contact sports like soccer, rugby, or wrestling.

- Wear tight, constrictive clothing with poor aeration.

- Have a weakened immune system (e.g., those infected with HIV or taking immunosuppressive drugs).

"P. brasiliensis" is a thermally dimorphic fungus distributed in Brazil and South America. The habitat of the infectious agent is not known, but appears to be aquatic. In biopsies, the fungus appears as a polygemulating yeast with a pilot's wheel-like appearance.

Paracoccidioidomycosis has been reported as an autochthonous disease from southern Mexico to northern Argentina. No cases have been reported from Belize and Nicaragua in Central America, or from Chile, French Guiana, Guiana, and Suriname in South America. Paracoccidioidomycosis is prevalent in Brazil, Colombia, Venezuela, and Argentina, and is classically associated with individuals from rural areas. The typical patient is a man aged 30 to 50 years.

Globally, fungal infections affect about 15% of the population and affects one out of five adults. Athlete's foot is common in individuals who wear occlusive shoes. Countries and regions where going barefoot is more common experience much lower rates of athlete's foot than do populations which habitually wear shoes; as a result, the disease has been called "a penalty of civilization". Studies have demonstrated that men are infected 2–4 times more often than women.

When the dermatophytic infection presents in wrestlers, with skin lesions typically found on the head, neck, and arms it is sometimes called tinea corporis gladiatorum.

In most cases, the prognosis of mucormycosis is poor and has varied mortality rates depending on its form and severity. In the rhinocerebral form, the mortality rate is between 30% and 70%, whereas disseminated mucormycosis presents with the highest mortality rate in an otherwise healthy patient, with a mortality rate of up to 90%. Patients with AIDS have a mortality rate of almost 100%. Possible complications of mucormycosis include the partial loss of neurological function, blindness and clotting of brain or lung vessels.

Mucormycosis is a very rare infection, and as such, it is hard to note histories of patients and incidence of the infection. However, one American oncology center revealed that mucormycosis was found in 0.7% of autopsies and roughly 20 patients per every 100,000 admissions to that center. In the United States, mucormycosis was most commonly found in rhinocerebral form, almost always with hyperglycemia and metabolic acidosis (e.g. DKA). In most cases the patient is immunocompromised, although rare cases have occurred in which the subject was not; these are usually due to a traumatic inoculation of fungal spores. Internationally, mucormycosis was found in 1% of patients with acute leukemia in an Italian review.

Unlike most other manifestations of Tinea dermatophyte infections, Kerion is not sufficiently treated with topical antifungals and requires systemic therapy. Typical therapy consists of oral antifungals, such as griseofulvin or terbinafine, for a sustained duration of at least 6-8 weeks depending on severity. Successful treatment of kerion often requires empiric bacterial antibiotics given the high prevalence of secondary bacterial infection.

Advice often given includes:

- Avoid sharing clothing, sports equipment, towels, or sheets.

- Wash clothes in hot water with fungicidal soap after suspected exposure to ringworm.

- Avoid walking barefoot; instead wear appropriate protective shoes in locker rooms and sandals at the beach.

- Avoid touching pets with bald spots, as they are often carriers of the fungus.

Historically, there have been many types of dermatophytes that were known to cause Majocchi's granuloma. Trichophyton violaceum used to be one of the most common species of dermatophytes to cause this disease. Today, however, Trichophyton rubrum proves to be the main culprit is most cases. These fungi are keratinophilic and colonize or infect the superficial keratinized tissues (the skin, nails, and hair) of humans and animals. The organisms are usually restricted to the non-living cornified layer of the epidermis and do not invade beyond the epidermis. The fungi are usually unable to penetrate into viable tissues in a immunocompetent host and therefore many times the infection incidence is higher in immune compromised individuals. There are two forms of MG: (i) the small, perifollicular papular form, which is a localized dermal infection that usually occurs in healthy individuals and (ii) the form featuring deep subcutaneous plaques or nodular lesions that occur in immunosuppressed hosts. Tinea corporis is the name of the subset of this disease that only remains restricted to the stratum corneum. Otherwise, the atypical deeper involvement is known as Majocchi's granuloma. Because keratinophilic dermatophytes digest keratin, the introduction of keratin into the dermis may also act as a medium for continued growth of the organism.

Tinea capitis caused by species of "Microsporum" and "Trichophyton" is a contagious disease that is endemic in many countries. Affecting primarily pre-pubertal children between 6 and 10 years, it is more common in males than females; rarely does the disease persist past age sixteen. Because spread is thought to occur through direct contact with afflicted individuals, large outbreaks have been known to occur in schools and other places where children are in close quarters; however, indirect spread through contamination with infected objects ("fomites") may also be a factor in the spread of infection. In the USA, tinea capitis is thought to occur in 3-8% of the pediatric population; up to one-third of households with contact with an infected person may harbor the disease without showing any symptoms.

The fungal species responsible for causing tinea capitis vary according to the geographical region, and may also change over time. For example, "Microsporum audouinii" was the predominant etiological agent in North America and Europe until the 1950s, but now "Trichophyton tonsurans" is more common in the USA, and becoming more common in Europe and the United Kingdom. This shift is thought to be due to the widespread use of griseofulvin, which is more effective against "M. audounii" than "T. tonsurans"; also, changes in immigration patterns and increases in international travel have likely spread "T. tonsurans" to new areas. Another fungal species that has increased in prevalence is "Trichophyton violaceum", especially in urban populations of the United Kingdom and Europe.

According to the National Health Service, "Athlete’s foot is very contagious and can be spread through direct and indirect contact." The disease may spread to others directly when they touch the infection. People can contract the disease indirectly by coming into contact with contaminated items (clothes, towels, etc.) or surfaces (such as bathroom, shower, or locker room floors). The fungi that cause athlete's foot can easily spread to one's environment. Fungi rub off of fingers and bare feet, but also travel on the dead skin cells that continually fall off the body. Athlete's foot fungi and infested skin particles and flakes may spread to socks, shoes, clothes, to other people, pets (via petting), bed sheets, bathtubs, showers, sinks, counters, towels, rugs, floors, and carpets.

When the fungus has spread to pets, it can subsequently spread to the hands and fingers of people who pet them. If a pet frequently gnaws upon itself, it might not be fleas it is reacting to, it may be the insatiable itch of tinea.

One way to contract athlete's foot is to get a fungal infection somewhere else on the body first. The fungi causing athlete's foot may spread from other areas of the body to the feet, usually by touching or scratching the affected area, thereby getting the fungus on the fingers, and then touching or scratching the feet. While the fungus remains the same, the name of the condition changes based on where on the body the infection is located. For example, the infection is known as tinea corporis ("ringworm") when the torso or limbs are affected or tinea cruris (jock itch or dhobi itch) when the groin is affected. Clothes (or shoes), body heat, and sweat can keep the skin warm and moist, just the environment the fungus needs to thrive.

no approved human vaccine exist against "Dermatophytosis". For horses, dogs and cats there is available an approved inactivated vaccine called "Insol Dermatophyton" (Boehringer Ingelheim) which provides time-limited protection against several trichophyton and microsporum fungal strains.

Pathogenic zygomycosis is caused by species in two orders: Mucorales or Entomophthorales, with the former causing far more disease than the latter. These diseases are known as "mucormycosis" and "entomophthoramycosis", respectively.

- Order Mucorales (mucormycosis)

- Family Mucoraceae

- "Absidia" ("Absidia corymbifera")

- "Apophysomyces" ("Apophysomyces elegans" and "Apophysomyces trapeziformis")

- "Mucor" ("Mucor indicus")

- "Rhizomucor" ("Rhizomucor pusillus")

- "Rhizopus" ("Rhizopus oryzae")

- Family Cunninghamellaceae

- "Cunninghamella" ("Cunninghamella bertholletiae")

- Family Thamnidiaceae

- "Cokeromyces" ("Cokeromyces recurvatus")

- Family Saksenaeaceae

- "Saksenaea" ("Saksenaea vasiformis")

- Family Syncephalastraceae

- "Syncephalastrum" ("Syncephalastrum racemosum")

- Order Entomophthorales (entomophthoramycosis)

- Family Basidiobolaceae

- "Basidiobolus" ("Basidiobolus ranarum")

- Family Ancylistaceae

- "Conidiobolus" ("Conidiobolus coronatus/Conidiobolus incongruus")

Opportunistic infections (infections that are caused by a diminished immune system) are frequent. Fungus from an athlete's foot infection can spread to the groin through clothing. Tight, restrictive clothing, such as jockstraps, traps heat and moisture, providing an ideal environment for the fungus.

The type of fungus involved is usually "Trichophyton rubrum". Some other contributing fungi are "Candida albicans", "Trichophyton mentagrophytes" and "Epidermophyton floccosum".

Acute paronychia is usually caused by bacteria. Claims have also been made that the popular acne medication, isotretinoin, has caused paronychia to develop in patients. Paronychia is often treated with antibiotics, either topical or oral. Chronic paronychia is most often caused by a yeast infection of the soft tissues around the nail but can also be traced to a bacterial infection. If the infection is continuous, the cause is often fungal and needs antifungal cream or paint to be treated.

Risk factors include repeatedly washing hands and trauma to the cuticle such as may occur from biting. In the context of bartending, it is known as "bar rot".

Prosector's paronychia is a primary inoculation of tuberculosis of the skin and nails, named after its association with prosectors, who prepare specimens for dissection. Paronychia around the entire nail is sometimes referred to as "runaround paronychia".

Painful paronychia in association with a scaly, erythematous, keratotic rash (papules and plaques) of the ears, nose, fingers, and toes may be indicative of acrokeratosis paraneoplastica, which is associated with squamous cell carcinoma of the larynx.

Paronychia can occur with diabetes, drug-induced immunosuppression, or systemic diseases such as pemphigus.

Filamentous fungi

- Aspergillus flavus

- Aspergillus fumigatus

- Fusarium spp.

- Alternaria spp.

- Curvularia

- Acremonium

Yeasts

- Candida

Fusarium spp. is most common then Aspergillus spp. and thirdly Dematitious fungi causing fungal keratitis in India.

The immune reconstitution inflammatory syndrome (IRIS) has been described in those with normal immune function with meningitis caused by "C. gattii" and "C. grubii". Several weeks or even months into appropriate treatment, there can be deterioration with worsening meningitis symptoms and progression or development of new neurological symptoms. IRIS is however much more common in those with poor immune function (≈25% vs. ≈8%).

Magnetic resonance imaging shows increase in the size of brain lesions, and CSF abnormalities (white cell count, protein, glucose) increase. Radiographic appearance of cryptococcal IRIS brain lesions can mimic that of toxoplasmosis with ring enhancing lesions on head computed tomography (CT). CSF culture is sterile, and there is no increase in CSF cryptococcal antigen titre.

The increasing inflammation can cause brain injury or be fatal.

The mechanism behind IRIS in cryptococcal meningitis is primarily immunologic. With reversal of immunosuppression, there is paradoxical increased inflammation as the recovering immune system recognises the fungus. In severe IRIS cases, treatment with systemic corticosteroids has been utilized - although evidence-based data are lacking.