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

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.

"Candida" yeasts are generally present in healthy humans, frequently part of the human body's normal oral and intestinal flora, and particularly on the skin; however, their growth is normally limited by the human immune system and by competition of other microorganisms, such as bacteria occupying the same locations in the human body.

"Candida" requires moisture for growth, notably on the skin. For example, wearing wet swimwear for long periods of time is believed to be a risk factor. In extreme cases, superficial infections of the skin or mucous membranes may enter into the bloodstream and cause systemic "Candida" infections.

Factors that increase the risk of candidiasis include HIV/AIDS, mononucleosis, cancer treatments, steroids, stress, antibiotic usage, diabetes, and nutrient deficiency. Hormone replacement therapy and infertility treatments may also be predisposing factors. Treatment with antibiotics can lead to eliminating the yeast's natural competitors for resources in the oral and intestinal flora; thereby increasing the severity of the condition. A weakened or undeveloped immune system or metabolic illnesses are significant predisposing factors of candidiasis. Almost 15% of people with weakened immune systems develop a systemic illness caused by "Candida" species. Diets high in simple carbohydrates have been found to affect rates of oral candidiases.

"C. albicans" was isolated from the vaginas of 19% of apparently healthy women, i.e., those who experienced few or no symptoms of infection. External use of detergents or douches or internal disturbances (hormonal or physiological) can perturb the normal vaginal flora, consisting of lactic acid bacteria, such as lactobacilli, and result in an overgrowth of "Candida" cells, causing symptoms of infection, such as local inflammation. Pregnancy and the use of oral contraceptives have been reported as risk factors. Diabetes mellitus and the use of antibiotics are also linked to increased rates of yeast infections.

In penile candidiasis, the causes include sexual intercourse with an infected individual, low immunity, antibiotics, and diabetes. Male genital yeast infections are less common, but a yeast infection on the penis caused from direct contact via sexual intercourse with an infected partner is not uncommon.

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.

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)

Invasive candidiasis is caused by 15 of the more than 150 known species of "Candida". These species, all confirmed by isolation from patients, are: C. albicans, "C. glabrata", "C. tropicalis", "C. parapsilosis", "C. krusei", "C. guilliermondii", "C. lusitaniae", "C. dubliniensis", "C. pelliculosa", "C. kefyr", "C. lipolytica", C. famata, "C. inconspicua", "C. rugosa", and "C. norvegensis". Over the last 20 – 30 years, "C. albicans" has been responsible for 95% of infections, with, "C. glabrata", "C. parapsilosis", "C. tropicalis", and "C. krusei" causing the majority of the remaining cases. Recently, "C. auris", a species first reported in 2009, has been found to cause invasive candidiasis. "C. auris" has attracted attention because it can be resistant to the antifungal medications used to treat candidiasis.

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.

Patients with esophageal candidiasis present with odynophagia, or painful swallowing. Longstanding esophageal candidiasis can result in weight loss. There is often concomittant thrush.

Some patients present with esophageal candidiasis as a first presentation of systemic candidiasis.

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

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).

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.

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.

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 white appearance is created by hyperkeratosis (overproduction of keratin) and epithelial hyperplasia. The causative agent implicated is Epstein-Barr virus, the same virus that causes infectious mononucleosis (glandular fever). After the primary EBV infection has been overcome, the virus will persist for the rest of the host's life and "hides" from the immune system by latent infection of B lymphocytes. The virus also causes lytic infection in the oropharynx, but is kept in check by a normal, functioning immune system. Uncontrolled lytic infection is manifested as oral hairy leukoplakia in immunocompromised hosts. OHL usually arises where the immunocompromise is secondary to HIV/AIDS. Rarely are other causes of immunocompromise associated with OHL, but it has been reported in people who have received transplants and are taking immunosuppressive medication. OHL may also accompany chronic graft versus host disease. Even more rare are reports of OHL in persons with competent immune systems.

Fungemia or fungaemia is the presence of fungi or yeasts in the blood. The most common type, also known as candidemia, candedemia, or systemic candidiasis, is caused by "Candida" species, but infections by other fungi, including "Saccharomyces", "Aspergillus" and "Cryptococcus", are also called fungemia. It is most commonly seen in immunosuppressed or immunocompromised patients with severe neutropenia, cancer patients, or in patients with intravenous catheters. It has been suggested the otherwise immunocompetent patients taking infliximab may be at a higher risk for fungemia.

Diagnosis is difficult, as routine blood cultures have poor sensitivity.

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.

Vaginitis is the disruption of the healthy vaginal microbiota. The vaginal microbiota consists of those organisms which generally do not cause symptoms, infections, and results in good pregnancy outcomes, and is dominated mainly by Lactobacillus species. The disruption of the normal microbiota can cause a vaginal yeast infection. Vaginal yeast infection can affect women of all ages and is very common. The yeast "Candida albicans" is the most common cause of vaginitis. Specific forms of vaginal inflammation include the following types:

Infectious vaginitis accounts for 90% of all cases in reproductive age women:

- Candidiasis: vaginitis caused by proliferation of "Candida albicans", "Candida tropicalis", "Candida krusei"

- Bacterial vaginosis: vaginitis caused by increased growth of "Gardnerella" (a bacterium).

- Aerobic vaginitis

Other less common infections are caused by gonorrhea, chlamydia, "Mycoplasma", herpes, "Campylobacter", improper hygiene, and some parasites, notably "Trichomonas vaginalis". Women who have diabetes develop infectious vaginitis more often than women who do not.

Vaginal infections often have multiple causes (varies between countries between 20 and 40% of vaginal infections), which present challenging cases for treatment. Indeed, when only one cause is treated, the other pathogens can become resistant to treatment and induce relapses and recurrences. Therefore, the key factor is to get a precise diagnosis and treat with broad spectrum anti-infective agents (often also inducing adverse effects).

Further, either a change in pH balance or introduction of foreign bacteria in the vagina can lead to infectious vaginitis. Physical factors that have been claimed to contribute to the development of infections include the following: constantly wet vulva due to tight clothing, chemicals coming in contact with the vagina via scented tampons, antibiotics, birth control pills, or a diet favoring refined sugar and yeast.

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.

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.

It is an uncommon condition, occurring with equal prevalence in males and females and at any age.

Enterocolitis or coloenteritis is an inflammation of the digestive tract, involving enteritis of the small intestine and colitis of the colon. It may be caused by various infections, with bacteria, viruses, fungi, parasites, or other causes. Common clinical manifestations of enterocolitis are frequent diarrheal defecations, with or without nausea, vomiting, abdominal pain, fever, chills, alteration of general condition. General manifestations are given by the dissemination of the infectious agent or its toxins throughout the body, or – most frequently – by significant losses of water and minerals, the consequence of diarrhea and vomiting.

Among the causal agents of acute enterocolitis are:

- bacteria: "Salmonella", "Shigella", "Escherichia coli", "Campylobacter" etc.;

- viruses: enteroviruses, rotaviruses, Norwalk virus, adenoviruses;

- fungi: candidiasis, especially in immunosuppressed patients or who have previously received prolonged antibiotic treatment;

- parasites: "Giardia lamblia" (with high frequency of infestation in the population, but not always with clinical manifestations), "Balantidium coli", "Blastocystis homnis", "Cryptosporidium" (diarrhea in people with immunosuppression), "Entamoeba histolytica" (produces the amebian dysentery, common in tropical areas).

Predisposing factors include smoking, denture wearing, use of corticosteroid sprays or inhalers and human immunodeficiency virus (HIV) infection. "Candida" species even in healthy people mainly colonizes the posterior dorsal tongue. Median rhombiod glossitis is thought to be a type of chronic atrophic (or erythematous) candidiasis. Microbiological culture of the lesion usually shows "Candida" mixed with bacteria.

Bumblefoot is a common infection for domesticated poultry and waterfowl such as chickens, ducks and quail. Due to constant walking on hard, rough, or sharp surfaces, birds can develop small wounds on the bottom of their feet. These wounds are very susceptible to infection by opportunistic bacterial pathogens, chiefly "Staphylococcus aureus". Treatment often requires opening the wound to drain the pus, soaking it in epsom salts, and antibiotic treatment and local application of the antiseptic pyodine as local dressing.