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.

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.

The prognosis for chromoblastomycosis is very good for small lesions. Severe cases are difficult to cure, although the prognosis is still quite good. The primary complications are ulceration, lymphedema, and secondary bacterial infection. A few cases of malignant transformation to squamous cell carcinoma have been reported. Chromoblastomycosis is very rarely fatal.

"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.

It is rare for the disease to appear before age 20, and it appears to be noticeably more common in males than females, especially over the age of 50, where the incidence of the disease (the risk per person in the population) does increase. The average age of onset is between 45 and 55 years of age for patients with patch and plaque disease only, but is over 60 for patients who present with tumours, erythroderma (red skin) or a leukemic form (the Sézary syndrome). The incidence of mycosis fungoides was seen to be increasing till the year 2000 in the United States, thought to be due to improvements in diagnostics. However, the reported incidence of the disease has since then remained constant, suggesting another unknown reason for the jump seen before 2000.

Treatment for phycomycosis is very difficult and includes surgery when possible. Postoperative recurrence is common. Antifungal drugs show only limited effect on the disease, but itraconazole and terbinafine hydrochloride are often used for two to three months following surgery. Humans with "Basidiobolus" infections have been treated with amphotericin B and potassium iodide. For pythiosis and lagenidiosis, a new drug targeting water moulds called caspofungin is available, but it is very expensive. Immunotherapy has been used successfully in humans and horses with pythiosis. Treatment for skin lesions is traditionally with potassium iodide, but itraconazole has also been used successfully.

Entomophthoramycosis (or Entomophthoromycosis) is a mycosis caused by Entomophthorales.

Examples include basidiobolomycosis and conidiobolomycosis.

Smoking, especially heavy smoking, is an important predisposing factor but the reasons for this relationship are unknown. One hypothesis is that cigarette smoke contains nutritional factors for "C. albicans", or that local epithelial alterations occur that facilitate colonization of candida species.

Malnutrition, whether by malabsorption, or poor diet, especially hematinic deficiencies (iron, vitamin B12, folic acid) can predispose to oral candidiasis, by causing diminished host defense and epithelial integrity. For example, iron deficiency anemia is thought to cause depressed cell-mediated immunity. Some sources state that deficiencies of vitamin A or pyridoxine are also linked.

There is limited evidence that a diet high in carbohydrates predisposes to oral candidiasis. "In vitro" and studies show that Candidal growth, adhesion and biofilm formation is enhanced by the presence of carbohydrates such as glucose, galactose and sucrose.

The most common method of treatment includes radiotherapy and/or surgical excision .

Drug-induced pseudolymphoma results from exposure to medications, which results in cutaneous inflammatory patterns that resemble lymphoma, most frequently mycosis fungoides.

The cause of mycosis fungoides is unknown, but it is not believed to be hereditary or genetic in the vast majority of cases. One incident has been reported of a possible genetic link. It is not contagious.

The disease is an unusual expression of CD4 T cells, a part of the immune system. These T cells are skin-associated, meaning that they biochemically and biologically are most related to the skin, in a dynamic manner. Mycosis fungoides is the most common type of cutaneous T-cell lymphoma (CTCL), but there are many other types of CTCL that have nothing to do with mycosis fungoides and these disorders are treated differently.

The disease is endemic in tropical and subtropical regions. The exact incidence and geographical distribution of mycetoma throughout the world is not known as the disease is usually painless, slowly progressive and presented to health centres only in late stages by majority of patients. Mycetoma has an uneven worldwide distribution.

White piedra (or tinea blanca) is a mycosis of the hair caused by several species of fungi in the genus "Trichosporon". It is characterized by soft nodules composed of yeast cells and arthroconidia that encompass hair shafts.

Pagetoid reticulosis (also known as "acral mycoses fungoides", "localized epidermotropic reticulosis", "mycosis fungoides palmaris et plantaris", "unilesional mycosis fungoides", and "Woringer–Kolopp disease") is a cutaneous condition, an uncommon lymphoproliferative disorder, sometimes considered a form of mycosis fungoides.

One approach involves shaving the affected areas. Another approach involves the use of antifungal medication.

The following clinical conditions may be considered before diagnosing a patient with mycetoma:

1. Tuberculous ulcer

2. Kaposi's sarcoma, a vascular tumour of skin usually seen in AIDS.

3. Leprosy

4. Syphilis

5. Malignant neoplasm

6. Tropical ulcer

7. Botryomycosis, a skin infection usually caused by the bacteria Staphylococcus aureus.

Non-mycosis fungoides CD30− cutaneous large T-cell lymphoma is a cutaneous condition that usually presents as solitary or generalized plaques, nodules, or tumors of short duration.

Although it is classified as a protozoal disease in ICD-10, their phylogenetic placement has been resolved to be within the Fungi, and some sources classify microsporidiosis as a mycosis, however, they are highly divergent and rapidly evolving.

Poikiloderma vasculare atrophicans (PVA), sometimes referred to as parapsoriasis variegata or parapsoriasis lichenoides is a cutaneous condition (skin disease) characterized by hypo- or hyperpigmentation (diminished or heightened skin pigmentation, respectively), telangiectasia and skin . Other names for the condition include prereticulotic poikiloderma and atrophic parapsoriasis. The condition was first described by pioneer American pediatrician Abraham Jacobi in 1906. PVA causes areas of affected skin to appear speckled red and inflamed, yellowish and/or brown, gray or grayish-black, with scaling and a thinness that may be described as "cigarette paper". On the surface of the skin, these areas may range in size from small patches, to plaques (larger, raised areas), to neoplasms (spreading, tumor-like growths on the skin).

Mycosis fungoides, a type of skin lymphoma, may be a cause of PVA. The condition may also be caused by, associated with or accompany any of the following conditions or disorders: other skin lymphomas, dermatomyositis, lupus erythematosus, Rothmund-Thompson syndrome, Kindler syndrome, dyskeratosis congenita, and chronic radiodermatitis. Rare causes include arsenic ingestion, and the condition can also be idiopathic.

PVA may be considered a rare variant of cutaneous T-cell lymphoma, a non-Hodgkin's form of lymphoma affecting the skin. It may also be included among a number of similar conditions that are considered as precursors to mycosis fungoides. PVA is believed to be a syndrome closely associated with large-plaque parapsoriasis and its cohort retiform parapsoriasis; including PVA, all three conditions fit within an updated view of the once ambiguous classification scheme known as parapsoriasis.

Fumagillin has been used in the treatment.

Another agent used is albendazole.

PVA usually has an underlying cause, attributed to existing skin diseases and disorders associated with a cutaneous lymphoma or inflammation. Mycosis fungoides is the common lymphoma believed to cause PVA, although it may be considered a precursor when the lymphoma is (hidden) and undiagnosed. Large plaque parapsoriasis is another common causes of PVA. Less common causes include autoimmune-related connective tissue diseases such as lupus, dermatomyositis and scleroderma. Dermatoses and those that are genetically inspired, called genodermatoses, may also be an underlying cause of PVA. Among them, xeroderma pigmentosum and Rothmund-Thomson syndrome (poikiloderma congenita) are thought to be the most prominent. Ingestion of substances containing arsenic, such as arsphenamine, has also been suggested as a least common cause. PVA can also be idiopathic (of unknown cause), as seen in a small number of cases.

Jessner lymphocytic infiltrate of the skin is a cutaneous condition characterized by a persistent papular and plaque-like skin eruption which can occur on the neck, face and back and may re-occur. This is an uncommon skin disease and is a benign collection of lymph cells. Its cause is not known and can be hereditary. It is named for Max Jessner. It is thought to be equivalent to lupus erythematosus tumidus.

It can occur as the result of ACE inhibitors and a number of medications used to treat multiple sclerosis including glatiramer acetate.