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.

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

A diet that supports the immune system and is not high in simple carbohydrates contributes to a healthy balance of the oral and intestinal flora. While yeast infections are associated with diabetes, the level of blood sugar control may not affect the risk. Wearing cotton underwear may help to reduce the risk of developing skin and vaginal yeast infections, along with not wearing wet clothes for long periods of time.

Oral hygiene can help prevent oral candidiasis when people have a weakened immune system. For people undergoing cancer treatment, chlorhexidine mouthwash can prevent or reduce thrush. People who use inhaled corticosteroids can reduce the risk of developing oral candidiasis by rinsing the mouth with water or mouthwash after using the inhaler.

For women who experience recurrent yeast infections, there is limited evidence that oral or intravaginal probiotics help to prevent future infections. This includes either as pills or as yogurt.

Several drugs may cause AC as a side effect, by various mechanisms, such as creating drug-induced xerostomia. Various examples include isotretinoin, indinavir, and sorafenib. Isotretinoin (Accutane), an analog of vitamin A, is a medication which dries the skin. Less commonly, angular cheilitis is associated with primary hypervitaminosis A, which can occur when large amounts of liver (including cod liver oil and other fish oils) are regularly consumed or as a result from an excess intake of vitamin A in the form of vitamin supplements. Recreational drug users may develop AC. Examples include cocaine, methamphetamines, heroin, and hallucinogens.

While infections may occur without sex, a high frequency of intercourse increases the risk. Personal hygiene methods or tight-fitting clothing, such as tights and thong underwear, do not appear to increase the risk.

In pregnancy, higher levels of estrogen make a woman more likely to develop a yeast infection. During pregnancy, the "Candida" fungus is more common, and recurrent infection is also more likely. There is tentative evidence that treatment of asymptomatic candidal vulvovaginitis in pregnancy reduces the risk of preterm birth.

Some systemic disorders are involved in angular cheilitis by virtue of their association with malabsorption and the creation of nutritional deficiencies described above. Such examples include people with anorexia nervosa. Other disorders may cause lip enlargement (e.g. orofacial granulomatosis), which alters the local anatomy and extenuates the skin folds at the corners of the mouth. More still may be involved because they affect the immune system, allowing normally harmless organisms like Candida to become pathogenic and cause an infection. Xerostomia (dry mouth) is thought to account for about 5% of cases of AC. Xerostomia itself has many possible causes, but commonly the cause may be side effects of medications, or conditions such as Sjögren's syndrome. Conversely, conditions which cause drooling or sialorrhoea (excessive salivation) can cause angular cheilitis by creating a constant wet environment in the corners of the mouth. About 25% of people with Down syndrome appear to have AC. This is due to relative macroglossia, an apparently large tongue in a small mouth, which may constantly stick out of the mouth causing maceration of the corners of the mouth with saliva. Inflammatory bowel diseases (such as Crohn's disease or ulcerative colitis) can be associated with angular cheilitis. In Crohn's, it is likely the result of malabsorption and immunosuppressive therapy which gives rise to the sores at the corner of the mouth. Glucagonomas are rare pancreatic endocrine tumors which secrete glucagon, and cause a syndrome of dermatitis, glucose intolerance, weight loss and anemia. AC is a common feature of glucagonoma syndrome. Infrequently, angular cheilitis may be one of the manifestations of chronic mucocutaneous candidiasis, and sometimes cases of oropharyngeal or esophageal candidiasis may accompany angular cheilitis. Angular cheilitis may be present in human immunodeficiency virus infection, neutropenia, or diabetes. Angular cheilitis is more common in people with eczema because their skin is more sensitive to irritants. Other conditions possibly associated include plasma cell gingivitis, Melkersson-Rosenthal syndrome, or sideropenic dysphagia (also called Plummer-Vinson syndrome or Paterson-Brown-Kelly syndrome).

Esophageal candidiasis is an opportunistic infection of the esophagus by "Candida albicans". The disease usually occurs in patients in immunocompromised states, including post-chemotherapy and in AIDS. However, it can also occur in patients with no predisposing risk factors, and is more likely to be asymptomatic in those patients. It is also known as candidal esophagitis or monilial esophagitis.

Denture-related stomatitis is usually a harmless condition with no long term consequences. It usually resolves with simple measures such as improved denture hygiene or topical antifungal medication. In severely immunocompromised individuals (e.g. those with HIV), the infection may present a more serious threat.

The major risk factor for the development of this condition is wearing an upper complete denture, particularly when it is not removed during sleep and cleaned regularly. Older dentures are more likely to be involved. Other factors include xerostomia (dry mouth), diabetes or a high carbohydrate diet. Human immunodeficiency virus (HIV) can rarely be an underlying factor.

Wearing dental appliances such as dentures alters the oral microbiota. A microbial plaque composed of bacteria and/or yeasts forms on the fitting surface of the denture (the surface which rests against the palate) and on the mucosa which is covered. Over time, this plaque may be colonized by Candida species. The local environment under a denture is more acidic and less exposed to the cleansing action of saliva, which favors high Candida enzymatic activity and may cause inflammation in the mucosa. "C. albicans" is the most commonly isolated organism, but occasionally bacteria are implicated.

There is controversy as to whether this condition represents a true infection by "C. albicans" or just a reaction to the various micro-organisms present underneath a denture. It has been reported that often the surface of the denture shows positive culture for "Candida" but biospsies of the mucosa rarely show hyphae invading epithelium. Similarly, microbiologic swabs of the involved mucosa show a much less heavy colonization than the surface of the denture. This has led some to conclude that the defining feature of a true infection is absent in denture-related stomatitis.

Poorly fitting dentures may cause pressure on the mucosa and mechanical irritation may create a similar clinical appearance, but this is uncommon. An orthodontic appliance may uncommonly produce a similar result. However, mucosal trauma is thought increase the ability of "C. albicans" to invade the tissues.

Aside from infection and mechanical trauma, inflammatory reactions of the mucosa beneath a denture can also result from irritation or allergy (allergic contact stomatitis) caused by the materials in the denture itself (acrylic, cobalt, chromium), or in response to substances within denture adhesives. Incomplete curing of the acrylic resin (the prosthetic material) may also be an involved factor.

Patients with the following conditions, treatments or situations are at increased risk for invasive candidiasis.

- Critical illness

- Long-term intensive care unit stay

- Abdominal surgery (aggravated by anastomotic leakage or repeat laparotomies)

- Immunosuppressive diseases

- Acute necrotizing pancreatitis

- Malignant hematologic disease

- Solid-organ transplantation

- Hematopoietic stem cell transplantation

- Solid-organ tumors

- Neonates (especially low birth weight and preterm infants)

- Broad-spectrum antibiotic treatment

- Central venous catheter

- Internal prosthetic device

- Total parenteral nutrition

- Hemodialysis

- Glucocorticoid use

- Chemotherapy

- Noninvasive "Candida" colonization (particularly if multifocal)

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

This is a common condition present in denture wearers. It appears as reddened but painless mucosa beneath the denture. 90% of cases are associated with Candidia species, and it is the most common form of oral candidiasis. Treatment is by antifungal medication and improved dental hygiene, such as not wearing the denture during sleep.

Allergic contact stomatitis (also termed "allergic gingivostomatitis" or "allergic contact gingivostomatitis") is a type IV (delayed) hypersensitivity reaction that occurs in susceptible atopic individuals when allergens penetrate the skin or mucosa.

Allergens, which may be different for different individuals, combine with epithelial-derived proteins, forming haptens which bind with Langerhans cells in the mucosa, which in turn present the antigen on their surface to T lymphocytes, sensitizing them to that antigen and causing them to produce many specific clones. The second time that specific antigen is encountered, an inflammatory reaction is triggered at the site of exposure. Allergic contact stomatitis is less common than allergic contact dermatitis because the mouth is coated in saliva, which washes away antigens and acts as a barrier. The oral mucosa is also more vascular (has a better blood supply) than skin, meaning that any antigens are more quickly removed from the area by the circulation. Finally, there is substantially less keratin in oral mucosa, meaning that there is less likelihood that haptens will form.

Allergic contact stomatitis appears as non-specific inflammation, so it may be mistaken for chronic physical irritation. There may be burning or soreness of the mouth and ulceration. Chronic exposure to the allergen may result in a lichenoid lesion. Plasma cell gingivitis may also occur, which may be accompanied by glossitis and cheilitis.

Allergens that may cause allergic contact stomatitis in some individuals include cinnamaldehyde, Balsam of Peru, peppermint, mercury, gold, pyrophosphates, zinc citrate, free acrylic monomer, nickel, fluoride, and sodium lauryl sulfate. These allergens may originate from many sources, including various foods and drink, chewing gum, toothpaste, mouthwash, dental floss, dental fillings, dentures, orthodontic bands or wires, and many other sources. If the substance containing the allergen comes into contact with the lips, allergic contact cheilitis can occur, together with allergic contact stomatitis.

The diagnosis is confirmed by patch test, and management is by avoidance of exposure to the allergen.

Invasive candidiasis is a nosocomial infection with the majority of cases associated with hospital stays.

In terms of the cause of chronic mucocutaneous candidiasis one finds it can be inherited either autosomal dominant or autosomal recessive There are 9 types of this condition with the first CANDF1 being located at 2p22.3-p21(cytogenetically)

Chronic mucocutaneous candidiasis is an immune disorder of T cells, it is characterized by chronic infections with "Candida" that are limited to mucosal surfaces, skin, and nails. It can also be associated with other types of infections, such as human papilloma virus. An association with chromosome 2 has been identified.

Tobacco smoking or chewing is the most common causative factor, with more than 80% of persons with leukoplakia having a positive smoking history. Smokers are much more likely to suffer from leukoplakia than non-smokers. The size and number of leukoplakia lesions in an individual is also correlated with the level of smoking and how long the habit has lasted for. Other sources argue that there is no evidence for a direct causative link between smoking and oral leukoplakia. Cigarette smoking may produce a diffuse leukoplakia of the buccal mucosa, lips, tongue and rarely the floor of mouth. Reverse smoking, where the lit end of the cigarette is held in the mouth is also associated with mucosal changes. Tobacco chewing, e.g. betel leaf and areca nut, called paan, tends to produce a distinctive white patch in a buccal sulcus termed "tobacco pouch keratosis". In the majority of persons, cessation triggers shrinkage or disappearance of the lesion, usually within the first year after stopping.

Although the synergistic effect of alcohol with smoking in the development of oral cancer is beyond doubt, there is no clear evidence that alcohol is involved in the development of leukoplakia, but it does appear to have some influence. Excessive use of a high alcohol containing mouth wash (> 25%) may cause a grey plaque to form on the buccal mucosa, but these lesions are not considered true leukoplakia.

Otomycosis is treated by debridment followed with topical azole antifungals, and symptomatically managed with oral antihistamines. Per a study in Iran 10cc acetic acid 2% plus 90 cc of isopropyl alcohol 70% was effective.

Candidal intertrigo is an infection of the skin by "Candida albicans", more specifically located between intertriginous folds of adjacent skin.

The most commonly known pathogen is "Candida albicans", causing roughly 70% of fungemias, followed by "Candida glabrata" with 10%, "Aspergillus" with 1% and "Saccharomyces" as the fourth most common. However, the frequency of infection by "C. glabrata", "Saccharomyces boulardii", "Candida tropicalis", "C. krusei" and "C. parapsilosis" is increasing, perhaps because significant use of fluconazole is common or due to increase in antibiotic use.

New emerging pathogen: "Candida auris" is an emerging multidrug-resistant (MDR) yeast that can cause invasive infections and is associated with high mortality. It was first described in 2009 after being isolated from external ear discharge of a patient in Japan. Since the 2009 report, C. auris infections, specifically fungemia, have been reported from South Korea, India, South Africa, and Kuwait. Although published reports are not available, C. auris has also been identified in Colombia, Venezuela, Pakistan, and the United Kingdom.

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

Vulvovaginitis in children may be "nonspecific", or caused by irritation with no known infectious cause, or infectious, caused by a pathogenic organism. Nonspecific vulvovaginitis may be triggered by fecal contamination, sexual abuse, chronic diseases, foreign bodies, nonestrogenized epithelium, chemical irritants, eczema, seborrhea, or immunodeficiency. It is treated with topical steroids; antibiotics may be given in cases where itching has resulted in a secondary infection.

Infectious vulvovaginitis can be caused by group A beta-hemolytic "Streptococcus" (7-20% of cases), "Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus, Shigella, Yersinia", or common STI organisms ("Neisseria gonorrhoeae, Chlamydia trachomatis, Trichomonas vaginalis", herpes simplex virus, and human papillomavirus)"." Symptoms and treatment of infectious vulvovaginitis vary depending on the organism causing it. "Shigella" infections of the reproductive tract usually coexist with infectious of the gastrointestinal tract and cause mucous, purulent discharge. They are treated with trimethoprim-sulfamethoxazole. "Streptococcus" infections cause similar symptoms to nonspecific vulvovaginitis and are treated with amoxicillin. STI-associated vulvovaginitis may be caused by sexual abuse or vertical transmission, and are treated and diagnosed like adult infections.