Symptoms of vaginal candidiasis are also present in the more common bacterial vaginosis; aerobic vaginitis is distinct and should be excluded in the differential diagnosis. In a 2002 study, only 33% of women who were self-treating for a yeast infection actually had such an infection, while most had either bacterial vaginosis or a mixed-type infection.

Diagnosis of a yeast infection is done either via microscopic examination or culturing. For identification by light microscopy, a scraping or swab of the affected area is placed on a microscope slide. A single drop of 10% potassium hydroxide (KOH) solution is then added to the specimen. The KOH dissolves the skin cells, but leaves the "Candida" cells intact, permitting visualization of pseudohyphae and budding yeast cells typical of many "Candida" species.

For the culturing method, a sterile swab is rubbed on the infected skin surface. The swab is then streaked on a culture medium. The culture is incubated at 37 °C (98.6 °F) for several days, to allow development of yeast or bacterial colonies. The characteristics (such as morphology and colour) of the colonies may allow initial diagnosis of the organism causing disease symptoms.

Respiratory, gastrointestinal, and esophageal candidiasis require an endoscopy to diagnose. For gastrointestinal candidiasis, it is necessary to obtain a 3–5 milliliter sample of fluid from the duodenum for fungal culture. The diagnosis of gastrointestinal candidiasis is based upon the culture containing in excess of 1,000 colony-forming units per milliliter.

Among individuals being treated in intensive care units, the mortality rate is about 30-50% when systemic candidiasis develops.

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.

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.

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.

Because many "Candida" species are part of the human microbiota, their presence in the mouth, the vagina, sputum, urine, stool, or skin is not definitive evidence for invasive candidiasis.

Positive culture of "Candida" species from normally sterile sites, such as blood, cerebrospinal fluid, pericardium, pericardial fluid, or biopsied tissue, is definitive evidence of invasive candidiasis. Diagnosis by culturing allows subsequent susceptibility testing of causitive species. Sensitivity of blood culture is far from ideal, with a sensitivity reported to be between 21 and 71%. Additionally, whereas blood culture can establish a diagnosis during fungemia, the blood may test negative for deep-seated infections because candida may have been successfully cleared from the blood.

Diagnosis of invasive candidiasis is supported by histopathologic evidence (for example, yeast cells or hyphae) observed in specimens of affected tissues.

Additionally, elevated serum β-glucan can demonstrate invasive candidiasis while a negative test suggests a low likelihood of systemic infection.

The emergence of multidrug-resistant "C. auris" as a cause of invasive candidiasis has necessitated additional testing in some settings. "C. auris"-caused invasive candidiasis is associated with high mortality. Many "C. auris" isolates have been found to be resistant to one or more of the three major antifungal classes (azoles, echinocandins, and polyenes) with some resistant to all three classes - severely limiting treatment options. Biochemical-based tests currently used in many laboratories to identify fungi, including API 20C AUX and VITEK-2, cannot differentiate "C. auris" from related species (for example, "C. auris" can be identified as "C. haemulonii"). Therefore, the Centers for Disease Control and Prevention recommends using a diagnostic method based on matrix-assisted laser desorption/ionization-time of flight mass spectrometry or a molecular method based on sequencing the D1-D2 region of the 28s rDNA to identify "C. auris" in settings were it may be present.

Preventative antifungal treatment is supported by studies, but only for specific high-risk groups in intensive care units with conditions that put them at high risk for the disease. For example, one group would be patients recovering from abdominal surgery that may have gastrointestinal perforations or anastomotic leakage. Antifungal prophylaxis can reduce the incidence of fungemia by approximately 50%, but has not been shown to improve survival. A major challenge limiting the number of patients receiving prophylaxis to only those that can potentially benefit, thereby avoiding the creation of selective pressure that can lead to the emergence of resistance.

The diagnosis is usually made based upon the clinical appearance, and swabs can be taken of the surface of the denture. Investigations to rule out possibility of diabetes may be indicated. Tissue biopsy is not usually indicated, but if taken shows histologic evidence of proliferative or degenerative responses and reduced keratinization and epithelial atrophy.

The current first-line treatment is fluconazole, 200 mg. on the first day, followed by daily dosing of 100 mg. for at least 21 days total. Treatment should continue for 14 days after relief of symptoms.

Other therapy options include:

- nystatin is not an effective treatment for esophageal candidiasis. It can be used as (swish, do not swallow) treatment for oral candidiasis that occurs with the use of asthma pumps.

- other oral triazoles, such as itraconazole

- caspofungin, used in refractory or systemic cases

- amphotericin, used in refractory or systemic cases

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).

Chronic mucocutaneous candidiasis can be diagnosed in an affected individual via the following methods/tests:

Angular chielitis is normally a diagnosis made clinically. If the sore is unilateral, rather than bilateral, this suggests a local factor ("e.g.", trauma) or a split syphilitic papule. Angular cheilitis caused by mandibular overclosure, drooling, and other irritants is usually bilateral.

The lesions are normally swabbed to detect if Candida or pathogenic bacterial species may be present. Persons with angular cheilitis who wear dentures often also will have their denture swabbed in addition. A complete blood count (full blood count) may be indicated, including assessment of the levels of iron, ferritin, vitamin B12 (and possibly other B vitamins), and folate.

Angular cheilitis could be considered to be a type of cheilitis or stomatitis. Where Candida species are involved, angular cheilitis is classed as a type of oral candidiasis, specifically a primary (group I) Candida-associated lesion. This form angular cheilitis which is caused by Candida is sometimes termed "Candida-associated angular cheilitis", or less commonly, "monilial perlèche". Angular cheilitis can also be classified as acute (sudden, short-lived appearance of the condition) or chronic (lasts a long time or keeps returning), or refractory (the condition persists despite attempts to treat it).

Diagnosis is typically suspected based on a women's symptoms. Diagnosis is made with microscopy (mostly by vaginal wet mount) and culture of the discharge after a careful history and physical examination have been completed. The color, consistency, acidity, and other characteristics of the discharge may be predictive of the causative agent. Determining the agent is especially important because women may have more than one infection, or have symptoms that overlap those of another infection, which dictates different treatment processes to cure the infection. For example, women often self-diagnose for yeast infections but due to the 89% misdiagnosis rate, self-diagnoses of vaginal infections are highly discouraged.

Another type of vaginitis, called desquamative inflammatory vaginitis (DIV) also exists. The cause behind this type is still poorly understood. DIV corresponds to the severe forms of aerobic vaginitis. About 5 to 10% of women are affected by aerobic vaginitis.

The International Statistical Classification of Diseases and Related Health Problems codes for the several causes of vaginitis are:

Prevention of candidiasis, the most common type of vaginitis, includes using loose cotton underwear. The vaginal area should be washed with water. Perfumed soaps, shower gels, and vaginal deodorants should be avoided. Douching is not recommended. The practice upsets the normal balance of yeast in the vagina and does more harm than good.

Prevention of bacterial vaginosis includes healthy diets and behaviors as well as minimizing stress as all these factors can affect the pH balance of the vagina.

Prevention of trichomoniasis revolves around avoiding other people's wet towels and hot tubs, and safe-sex procedures, such as condom use.

Some women consume good bacteria in food with live culture, such as yogurt, sauerkraut and kimchi, or in probiotic supplements either to try to prevent candidiasis, or to reduce the likelihood of developing bacterial vaginitis following antibiotic treatment. There is no firm evidence to suggest that eating live yogurt or taking probiotic supplements will prevent candidiasis.

Studies have suggested a possible clinical role for the use of standardized oral or vaginal probiotics in the treatment of bacterial vaginosis, either in addition to or in place of the typical antibiotic regimens. However, recent articles question their efficacy in preventing recurrence compared with other means, or conclude that there is insufficient evidence for or against recommending probiotics for the treatment of bacterial vaginosis.

Management for an individual with chronic mucocutaneous candidiasis consists of the following(relapse occurs once treatment is ceased, in many cases):

The most important aspect of treatment is improving denture hygiene, i.e. removing the denture at night, cleaning and disinfecting it, and storing it overnight in an antiseptic solution. This is important as the denture is usually infected with "C. albicans" which will cause re-infection if it is not removed. Substances which are used include solutions of alkaline peroxides, alkaline hypochlorites (e.g. hypochlorite, which may over time corrode metal components of dental appliances), acids (e.g. benzoic acid), yeast lytic enzymes and proteolytic enzymes (e.g. alcalase protease). The other aspect of treatment involves resolution of the mucosal infection, for which topical antifungal medications are used (e.g. nystatin, amphotericin, miconazole, fluconazole or itraconazole). Often an antimicrobial mouthwash such as chlorhexidine is concurrently prescribed. Possible underlying disease (diabetes, HIV) should be treated where possible.

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).

Neutropenic vs non-neutropenic candidemia is treated differently.

An intravenous echinocandin such as anidulafungin, caspofungin or micafungin is recommended as first-line therapy for fungemia, specifically candidemia. Oral or intravenous fluconazole is an acceptable alternative. The lipid formulation amphotericin B is a reasonable alternative if there is limited antifungal availability, antifungal resistance, or antifungal intolerance.

Intertrigo can be diagnosed clinically by a medical professional after taking a thorough history and performing a detailed physical examination. Many other skin conditions can mimic intertrigo's appearance including erythrasmascabies, pyoderma, atopic dermatitis, candidiasis, and seborrheic dermatitis, and fungal infections of the superficial skin caused by "Tinea versicolor" or "Tinea corporis".

The diagnosis is usually made on the clinical appearance, and tissue biopsy is not usually needed. The histologic picture is one of superficial candidal hyphal infiltration and a polymorphonuclear leukocytic inflammatory infiltrate present in the epithelium. The rete ridges are elongated and hyperplastic (pseudoepitheliomatous hyperplasia, which may be mistaken for carcinoma).

Intertrigo is treated by addressing associated infections, by removing moisture from the site, and by using substances at the site to help maintain skin integrity. If the individual is overweight, losing weight may also help. Relapses of intertrigo are common.

Keeping the area of the intertrigo dry and exposed to the air can help prevent recurrences, as can removing moisture from the area using absorbent fabrics or body powders, including plain cornstarch and judiciously used antiperspirants.

Greases, oils, and barrier ointments, may help by protecting skin from moisture and from friction. Antifungal powders, most commonly clotrimazole 1%, may also be used in conjunction with a barrier ointment. Diaper rash ointment can also help.

Fungal infections associated with intertrigo may be treated with prescription antifungals applied directly to the skin (in most cases) or systemic antifungals, including fluconazole, nystatin, and griseofulvin.

Intertrigo is also a known symptom of vitamin B6 deficiency.

The annual malignant transformation rate of leukoplakia rarely exceeds 1%, i.e. the vast majority of oral leukoplakia lesions will remain benign. A number of clinical and histopathologic features are associated with varying degrees of increased risk of malignant transformation, although other sources argue that there are no universally accepted and validated factors which can reliably predict malignant change. It is also unpredictable to an extent if an area of leukoplakia will disappear, shrink or remain stable.

- Presence and degree of dysplasia (mild, moderate or severe/carcinoma in situ). Dysplasia is the most important predictor of malignant change, and about 10% of leukoplakia lesions show dysplasia when biopsied.

- Leukoplakia located on the floor of the mouth, the posterior and lateral tongue, and the retromolar areas (the region behind the wisdom teeth) have higher risk, whereas white patches in areas such as the top surface of the tongue and the hard palate do not have significant risk. Although these "high risk" sites are recognized, statistically, leukoplakia is more common on the buccal mucosa, alveolar mucosa, and the lower labial mucosa. Leukoplakia of the floor of the mouth and tongue accounts for over 90% of leukoplakias showing dysplasia or carcinoma on biopsy. This is thought to be due to pooling of saliva in the lower part of the mouth, exposing these areas to more carcinogens held in suspension.

- Red lesions (erythroplasia) and mixed red and white lesions (erythroleukoplakia/"speckled leukoplakia") have a higher risk of malignant change than homogenous leukoplakia.

- Verrucous or nodular areas have a higher risk.

- Although smoking increases risk of malignant transformation, smoking also causes many white patches with no dysplasia. This means that statistically, white patches in non smokers have a higher risk.

- Older people with white patches are at higher risk.

- Larger white patches are more likely to undergo malignant transformation than smaller lesions.

- White patches which have been present for a long period of time have higher risk.

- Persons with a positive family history of cancer in the mouth.

- Candida infection in the presence of dysplasia has a small increased risk.

- A change in the appearance of the white patch, apart from a change in the color, has a higher risk. Changes in the lesion such as becoming fixed to underlying tissues, ulceration, cervical lymphadenopathy (enlargement of lymph nodes in the neck), and bone destruction may herald the appearance of malignancy.

- White patches present in combination with other conditions that carry a higher risk (e.g. oral submucous fibrosis), are more likely to turn malignant.

- Although overall, oral cancer is more common in males, females with white patches are at higher risk than men.

Tissue biopsy is usually indicated to rule out other causes of white patches and also to enable a detailed histologic examination to grade the presence of any epithelial dysplasia. This is an indicator of malignant potential and usually determines the management and recall interval. The sites of a leukoplakia lesion that are preferentially biopsied are the areas that show induration (hardening) and erythroplasia (redness), and erosive or ulcerated areas. These areas are more likely to show any dysplasia than homogenous white areas.

Brush biopsy/exfoliative cytology is an alternative to incisional biopsy, where a stiff brush is scraped against the lining of the mouth to remove a sample of cells. This is then made into a smear which can be examined microscopically. Sometimes the biopsy site can be selected with adjunct methods which aim to highlight areas of dysplasia. Toluidine blue staining, where the dye is preferentially retained by dysplastic tissue, is sometimes used, but there is high false positive rate. Other methods involve the use of illuminescence, relying on either the property of normal autoflorescent molecules in mucosa such as collagen and keratin which is lost from areas of dysplasia or carcinoma under blue light, or by initially staining of the mucosa with toluidine blue or dilute acetic acid and examination under white light.

Systemic candidiasis is an infection of Candida albicans causing disseminated disease and sepsis, invariably when host defenses are compromised.