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.

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

"Penicillium marneffei" demonstrates in vitro susceptibility to multiple antifungal agents including ketoconazole, itraconazole, miconazole, flucytosine, and amphotericin B. Without treatment patients have a poor prognosis; death occur by liver failure as the fungus releases toxins in the bloodstream. The elevation of liver enzyme in the blood helps to establish a diagnosis.

Diagnosis is often made by visualization of yeast cells in tissue, or superficial scrapings. Radiography of the chest reveals interstitial infiltrates in the majority of cases.

Cryptococcosis is a very subacute infection with a prolonged subclinical phase lasting weeks to months in persons with HIV/AIDS before the onset of symptomatic meningitis. In Sub-Saharan Africa, the prevalence rates of detectable cryptococcal antigen in peripheral blood is often 4–12% in persons with CD4 counts lower than 100 cells/mcL.

Cryptococcal antigen screen and preemptive treatment with fluconazole is cost saving to the healthcare system by avoiding cryptococcal meningitis. The World Health Organization recommends cryptococcal antigen screening in HIV-infected persons entering care with CD4<100 cells/μL. This undetected subclinical cryptococcal (if not preemptively treated with anti-fungal therapy) will often go on to develop cryptococcal meningitis, despite receiving HIV therapy. Cryptococcosis accounts for 20-25% of the mortality after initiating HIV therapy in Africa. What is effective preemptive treatment is unknown, with the current recommendations on dose and duration based on expert opinion. Screening in the United States is controversial, with official guidelines not recommending screening, despite cost-effectiveness and a 3% U.S. cryptococcal antigen prevalence in CD4<100 cells/μL.

Opportunistic infections caused by Feline Leukemia Virus and Feline immunodeficiency virus retroviral infections can be treated with Lymphocyte T-Cell Immune Modulator.

Dependent on the infectious syndrome, symptoms include fever, fatigue, dry cough, headache, blurred vision, and confusion. Symptom onset is often subacute, progressively worsened over several weeks. The two most common presentations are meningitis (an infection in and around the brain) and pulmonary (lung) infection.

Detection of cryptococcal antigen (capsular material) by culture of CSF, sputum and urine provides definitive diagnosis. Blood cultures may be positive in heavy infections. India ink of the CSF is a traditional microscopic method of diagnosis, although the sensitivity is poor in early infection, and may miss 15-20% of patients with culture-positive cryptococcal meningitis. Unusual morphological forms are rarely seen. Cryptococcal antigen from cerebrospinal fluid is the best test for diagnosis of cryptococcal meningitis in terms of sensitivity. Apart from conventional methods of detection like direct microscopy and culture, rapid diagnostic methods to detect cryptococcal antigen by latex agglutination test, lateral flow immunochromatographic assay (LFA), or enzyme immunoassay (EIA). A new cryptococcal antigen LFA was FDA approved in July 2011. Polymerase chain reaction (PCR) has been used on tissue specimens.

Cryptococcosis can rarely occur in the non-immunosuppressed people, particularly with "Cryptococcus gattii".

Diagnosis is usually made by identification of the fungi from clinical specimens. Biopsies of skin lesions, lymph nodes, and bone marrow demonstrate the presence of organisms on histopathology.

The most common symptoms are fever, skin lesions, anemia, generalized lymphadenopathy, and hepatomegaly.

Individuals at higher risk are often prescribed prophylactic medication to prevent an infection from occurring. A patient's risk level for developing an opportunistic infection is approximated using the patient's CD4 T-cell count and sometimes other markers of susceptibility. Common prophylaxis treatments include the following:

The white lesion cannot be wiped away, unlike some other common oral white lesions, e.g. pseudomembranous candidiasis, and this may aid in the diagnosis. Diagnosis of OHL is mainly clinical, but can be supported by proof of EBV in the lesion (achieved by in situ hybridization, polymerase chain reaction, immunohistochemistry, Southern blotting, or electron microscopy) and HIV serotesting. When clinical appearance alone is used to diagnose OHL, there is a false positive rate of 17% compared to more objective methods. The appearance of OHL in a person who is known to be infected with HIV does not usually require further diagnostic tests as the association is well known. OHL in persons with no known cause of immunocompromise usually triggers investigations to look for an underlying cause. If tissue biopsy is carried out, the histopathologic appearance is of hyperlastic and parakeratinized epithelium, with "balloon cells" (lightly staining cells) in the upper stratum spinosum and "nuclear beading" in the superficial layers (scattered cells with peripheral margination of chromatin and clear nuclei, created by displacement of chromatin to the peripheral nucleus by EBV replication). Candida usually is seen growing in the parakeratin layer, but there are no normal inflammatory reactions to this in the tissues. There is no dysplasia (OHL is not a premalignant lesion).

Fungal pneumonia can be diagnosed in a number of ways. The simplest and cheapest method is to culture the fungus from a patient's respiratory fluids. However, such tests are not only insensitive but take time to develop which is a major drawback because studies have shown that slow diagnosis of fungal pneumonia is linked to high mortality. Microscopy is another method but is also slow and imprecise. Supplementing these classical methods is the detection of antigens. This technique is significantly faster but can be less sensitive and specific than the classical methods.

A molecular test based on quantitative PCR is also available from Myconostica. Relying on DNA detection, this is the most sensitive and specific test available for fungi but it is limited to detecting only pneumocystis jirovecii and aspergillus.

Sulfonamides are the traditional remedies to paracoccidiodomycosis. They were introduced by Oliveira Ribeiro and used for more than 50 years with good results. The most-used sulfa drugs in this infection are sulfadimethoxime, sulfadiazine, and co-trimoxazole. This treatment is generally safe, but several adverse effects can appear, the most severe of which are the Stevens-Johnson syndrome and agranulocytosis. Similarly to tuberculosis treatment, it must be continued for up to three years to eradicate the fungus, and relapse and treatment failures are not unusual.

Antifungal drugs such as amphotericin B or itraconazole and ketoconazole are more effective in clearing the infection, but are limited by their cost when compared with sulfonamides.During therapy, fibrosis can appear and surgery may be needed to correct this. Another possible complication is Addisonian crisis. The mortality rate in children is around 7-10%.

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.

The diagnosis can typically be made from the clinical appearance alone, but not always. As candidiasis can be variable in appearance, and present with white, red or combined white and red lesions, the differential diagnosis can be extensive. In pseudomembraneous candidiasis, the membranous slough can be wiped away to reveal an erythematous surface underneath. This is helpful in distinguishing pseudomembraneous candidiasis from other white lesions in the mouth that cannot be wiped away, such as lichen planus, oral hairy leukoplakia. Erythematous candidiasis can mimic geographic tongue. Erythematous candidiasis usually has a diffuse border that helps distinguish it from erythroplakia, which normally has a sharply defined border.

Special investigations to detect the presence of candida species include oral swabs, oral rinse or oral smears. Smears are collected by gentle scraping of the lesion with a spatula or tongue blade and the resulting debris directly applied to a glass slide. Oral swabs are taken if culture is required. Some recommend that swabs be taken from 3 different oral sites. Oral rinse involves rinsing the mouth with phosphate-buffered saline for 1 minute and then spitting the solution into a vessel that examined in a pathology laboratory. Oral rinse technique can distinguish between commensal candidal carriage and candidiasis. If candidal leukoplakia is suspected, a biopsy may be indicated. Smears and biopsies are usually stained with periodic acid-Schiff, which stains carbohydrates in fungal cell walls in magenta. Gram staining is also used as Candida stains are strongly Gram positive.

Sometimes an underlying medical condition is sought, and this may include blood tests for full blood count and hematinics.

If a biopsy is taken, the histopathologic appearance can be variable depending upon the clinical type of candidiasis. Pseudomembranous candidiasis shows hyperplastic epithelium with a superficial parakeratotic desquamating (i.e., separating) layer. Hyphae penetrate to the depth of the stratum spinosum, and appear as weakly basophilic structures. Polymorphonuclear cells also infiltrate the epithelium, and chronic inflammatory cells infiltrate the lamina propria.

Atrophic candidiasis appears as thin, atrophic epithelium, which is non-keratinized. Hyphae are sparse, and inflammatory cell infiltration of the epithelium and the lamina propria. In essence, atrophic candidiasis appears like pseudomembranous candidiasis without the superficial desquamating layer.

Hyperplastic candidiasis is variable. Usually there is hyperplastic and acanthotic epithelium with parakeratosis. There is an inflammatory cell infiltrate and hyphae are visible. Unlike other forms of candidiasis, hyperplastic candidiasis may show dysplasia.

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.

Fumagillin has been used in the treatment.

Another agent used is albendazole.

In most cases the diagnosis is established based on response to therapy. Patients in whom esophageal candidiasis is suspected should receive a brief course of antifungal therapy with fluconazole. If the infection resolves after treatment with fluconazole, then the diagnosis of esophageal candidiasis is made and no further investigation is needed. However, if the infection persists or if there are other factors involved which may warrant further investigation, then patient will undergo an esophagogastroduodenoscopy if it is safe to do so. Endoscopy often reveals classic diffuse raised plaques that characteristically can be removed from the mucosa by the endsocope. Brushing or biopsy of the plaques shows yeast and pseudohyphae by histology that are characteristic of "Candida" species.

The severity of oral candidiasis is subject to great variability from one person to another and in the same person from one occasion to the next. The prognosis of such infection is usually excellent after the application of topical or systemic treatments. However, oral candidiasis can be recurrent. Individuals continue to be at risk of the condition if underlying factors such as reduced salivary flow rate or immunosuppression are not rectifiable.

Candidiasis can be a marker for underlying disease, so the overall prognosis may also be dependent upon this. For example, a transient erythematous candidiasis that developed after antiobiotic therapy usually resolves after antibiotics are stopped (but not always immediately), and therefore carries an excellent prognosis—but candidiasis may occasionally be a herald of a more sinister undiagnosed pathology, such as HIV/AIDS or leukemia.

It is possible for candidiasis to spread to/from the mouth, from sites such as the pharynx, esophagus, lungs, liver, anogenital region, skin or the nails. The spread of oral candidiasis to other sites usually occurs in debilitated individuals. It is also possible that candidiasis is spread by sexual contact. Rarely, a superficial candidal infection such as oral candidiasis can cause invasive candidiasis, and even prove fatal. The observation that Candida species are normally harmless commensals on the one hand, but are also occasionally capable of causing fatal invasive candidiases has led to the description "Dr Jekyll and Mr Hyde".

The role of thrush in the hospital and ventilated patients is not entirely clear however there is a theoretical risk of positive interaction of candida with topical bacteria that could increase the risk for Ventilator Associated Pneumonia and other diseases.

The oral lesion itself is benign and self-limiting, however this may not necessarily be the case for the underlying cause of immunocompromise. For instance, OHL with HIV/AIDS is a predictor of bad prognosis, (i.e. severe immunosuppression and advanced disease).

Fusariosis is an infection seen in neutropenic patients, and is a significant opportunistic pathogen in patients with hematologic malignancy.

It is associated with infections with "Fusarium" species, such as "Fusarium proliferatum".

In "Acanthamoeba" infections, the diagnosis can be made from microscopic examination of stained smears of biopsy specimens (brain tissue, skin, cornea) or of corneal scrapings, which may detect trophozoites and cysts. Cultivation of the causal organism, and its identification by direct immunofluorescent antibody, may also prove useful. Laboratory workers and physicians often mistake the organisms on wet mount for monocytes and a diagnosis of viral meningitis is mistakenly given if the organisms are not motile. Heating a copper penny with an alcohol lamp and placing it on the wet mount slide will activate sluggish trophozoites and more rapidly make the diagnosis. If the person performing the spinal tap rapidly looks at the heated wet mount slide the trophozoites can be seen to swarm while monocytes do not.

Fungal pneumonia can be treated with antifungal drugs and sometimes by surgical debridement.

A study conducted on 452 patients revealed that the genotype responsible for higher IL-10 expression makes HIV infected people more susceptible to tuberculosis infection. Another study on HIV-TB co-infected patients also concluded that higher level of IL-10 and IL-22 makes TB patient more susceptible to Immune reconstitution inflammatory syndrome (IRIS). It is also seen that HIV co-infection with tuberculosis also reduces concentration of immunopathogenic matrix metalloproteinase (MMPs) leading to reduced inflammatory immunopathology.

TS can be diagnosed based on clinical observations, but is usually confirmed by histopathology of a lesional biopsy or a plucked spicule. Characteristic histological findings include enlarged and abnormally organized hair follicles and hyperproliferation of inner root sheath cells containing large eosinophilic trichohyalin granules. Antibodies against major capsid protein VP1, the major component of the viral capsid, can be used to confirm the presence of viral particles in cell nuclei. Electron microscopy can also be used to detect viral particles. Quantification of viral load can be performed using quantitative PCR, as affected skin demonstrates much higher viral loads compared to unaffected skin or to asymptomatic individuals who test positive for viral DNA.

Differential diagnosis includes other visually similar conditions affecting the hair follicles, many of which appear as drug side effects. A proposed classification system lists TS as one of a group of cutaneous conditions with similar manifestations and distinct etiologies, collectively called the digitate keratoses. Although confirmed TS is very rare, the condition is thought to be underdiagnosed.

The diagnosis can be confirmed by the characteristic appearance of the chest x-ray, which shows widespread pulmonary infiltrates, and an arterial oxygen level (PaO) that is strikingly lower than would be expected from symptoms. Gallium 67 scans are also useful in the diagnosis. They are abnormal in approximately 90% of cases and are often positive before the chest x-ray becomes abnormal. The diagnosis can be definitively confirmed by histological identification of the causative organism in sputum or bronchio-alveolar lavage (lung rinse). Staining with toluidine blue, silver stain, periodic-acid schiff stain, or an immunofluorescence assay will show the characteristic cysts. The cysts resemble crushed ping-pong balls and are present in aggregates of 2 to 8 (and not to be confused with "Histoplasma" or "Cryptococcus", which typically do not form aggregates of spores or cells). A lung biopsy would show thickened alveolar septa with fluffy eosinophilic exudate in the alveoli. Both the thickened septa and the fluffy exudate contribute to dysfunctional diffusion capacity which is characteristic of this pneumonia.

"Pneumocystis" infection can also be diagnosed by immunofluorescent or histochemical staining of the specimen, and more recently by molecular analysis of polymerase chain reaction products comparing DNA samples. Notably, simple molecular detection of "Pneumocystis jirovecii" in lung fluids does not mean that a person has "Pneumocystis" pneumonia or infection by HIV. The fungus appears to be present in healthy individuals in the general population.