Systemic antibiotics are the most common cause of acute mucosal candidiasis. Oral exposure to topical glucocorticoid steroids is another common cause of medication-induced oral candidiasis, probably due to alterations of the local mucosal host immunity. Removal of the topical medication with water after exposure tends to prevent recurrence. General immune suppression due to systemic glucocorticoids, cancer chemotherapy and immunomodulators often causes mucosal candidiasis, which usually can be prevented by prophylactic antifungal treatment. Studies using both culture and pyrosequencing have shown that the oral mycobiota in immunosuppressed solid organ transplant recipients is dominated by Candida species (Charlson et al. 2012; Diaz et al. 2013; Dongari-Bagtzoglou et al. 2009). Salivary gland dysfunction resulting in reduced salivary flow rate (salivary hypofunction), compositional changes or a combination of both often has major consequences for the oral microbial balance and local immune defence leading to an increased risk of dental caries and oral candidiasis (Dawes et al. 2015). The main causes of salivary gland hypofunction are intake of medications, systemic diseases like Sjögren’s syndrome and head and neck radiotherapy (Villa et al. 2015; Jensen et al. 2010; Pedersen 2014).

A number of studies have shown that intake of xerogenic medication is associated with high rates of Candida carriage and oral candidiasis (Almståhl and Wikström 2003, 2005; Kaplan et al. 2008; Pedersen et al. 2015) (for further details, see Chap. 9).

The carriage frequency of Candida and the density of candidal colonization as well as the rates of oral Candida infections are increased in patients with both type 1 and type 2 diabetes mellitus (DM) (Tapper-Jones et al. 1981; Lamey et al. 1988, 1992; Hill et al. 1989; Vazques and Sobel 1995; Bai et al. 1995; Guggenheimer et al. 2000; Kadir et al. 2002; Jurevic et al 2003; Shenoy et al. 2014). Oral candidiasis is not only more common in patients with DM than in nondiabetics, the infections are also more severe (Guggenheimer et al. 2000). The increased susceptibility to oral candidiasis has been related to poor glycaemic control and hence high concentrations of glucose in the blood and saliva, long disease duration as well as presence of diabetic complications (retinopathy) (Bai et al. 1995; Bartholomew et al. 1987; Dorocka-Bobkowska et al. 1996; Guggenheimer et al. 2000; Kadir et al. 2002; Ueta et al. 1993; Vazques and Sobel 1995). High concentrations of glucose in the blood and saliva may promote growth and enhance adherence of yeasts to epithelial cell surfaces (Samaranayake 1990). Also the impaired functions of polymorphonuclear leukocytes leading to reduced phagocytosis, intracellular killing and chemotaxis may contribute to the increased colonization of Candida and increased susceptibility to oral candidiasis (Ueta et al. 1993; Vazques and Sobel 1995). However, other risk factors such as salivary gland hypofunction, low salivary pH and impaired salivary antimicrobial activity, poor oral hygiene, cigarette smoking and denture wearing also have a substantial influence on candidal colonization and various oral manifestations and symptoms of Candida infections in both type 1 and 2 DM patients (Budtz-Jørgensen 1990; Banoczy et al. 1987; Guggenheimer et al. 2000; Jurevic et al. 2003; Kadir et al. 2002; Pedersen 2004; Samaranayake 1990; Willis et al. 1999). Inadequately controlled diabetics who wear dentures have a higher oral candida load and higher prevalence of denture stomatitis than nondiabetic denture wearers (Guggenheimer et al. 2000; Vitkov et al. 1999).

C. albicans is the most common species isolated from the oral cavity of diabetics (Dorocka-Bobkowska et al. 1996; Kadir et al. 2002; Samaranayake 1990; Willis et al. 1999), but also C. dubliniensis, C. glabrata and C. tropicalis have been isolated from the oral cavity of patients with diabetes (Jurevic et al. 2003). The significance of species in relation to pathogenesis of fungal infections in diabetics remains to be elucidated.

Oral candidiasis is the most common opportunistic infection in HIV-infected patients and in patients with AIDS (Coleman et al. 1993; Shiboski et al. 2015) and one of the earliest indicators of the progression from HIV-seropositive status to AIDS. Oral candidiasis is strongly associated with immune suppression, as measured by CD4⁺ lymphocyte counts, and also associated with high viral burden and consequently suggested as a clinical marker of plasma viral load and the progression of HIV disease (Glick et al. 1994; Patton 2000).

The candida carriage in HIV-infected patients is predominated by C. albicans, but C. dubliniensis and C. glabrata have also commonly been isolated from oral lesions in HIV-infected patients (Sullivan et al. 1995; Li et al. 2007). The increased carriage of C. krusei has been associated with the widespread use of fluconazole prophylaxis (Samaranayke and Samaranayke 1994). A recent study on the oral mycobiome using pyrosequencing showed a shift in the oral mycobiome in which Epicoccum and Alternaria were abundantly colonizing HIV-infected patients, but Candida being abundant in both HIV patients and healthy subjects (Mukherjee et al. 2014).

The introduction of highly active antiretroviral therapy (HAART) has changed the epidemiology of oral candidiasis. Thus, several studies have reported a decrease in the prevalence and recurrence of oral candidiasis in HIV-infected patients receiving HAART (Greenspan et al. 2004; Jiang et al. 2014; Ramírez-Amador et al. 2007). However, some studies report rare cases of increased prevalence. There is substantial evidence suggesting that onset of oral candidiasis is associated with a progressive reduction in CD4⁺ lymphocyte count and an increase in viral load in HIV-infected patients receiving HAART (Hodgson et al. 2006; Ramírez-Amador et al. 2007). Oral candidiasis has therefore been suggested as a clinical marker of immune status and a predictor of virologic failure during HAART and hence an indicator of HIV disease progression and a tool for monitoring HIV infection in conjunction with CD4⁺ lymphocyte counts and plasma viral load in HIV-infected patients receiving HAART (Ramírez-Amador et al. 2007).

Recipients of solid organ transplants and haematopoietic cell transplants and patients receiving cancer therapy have a high risk of developing fungal infections due to immunosuppressive, immunomodulating therapy as well as treatment with antibiotics (Trenschel et al. 2000). Despite antifungal prophylaxis, the increased risk for systemic and oropharyngeal fungal infection is still a matter of concern in these patients, and fungal infections remain a significant cause of morbidity and mortality. The prevalence of oral candidiasis in renal transplant recipients ranges from 9.4 to 46.7 % (Al-Mohaya et al. 2002; de la Rosa-García et al. 2005; Güleç et al. 2003).

C. albicans has been found to be the most prevalent species isolated from the oral cavity of recipients of kidney transplants (da Silva-Rocha et al. 2014). Also in recipients of liver transplants, the Candida carriage and prevalence of oral candidiasis are high (40–50 %), and many of these patients also suffer from salivary gland hypofunction (Helenius-Hietala et al. 2014).

The most common forms of oral candidiasis reported in patients receiving cancer therapy are pseudomembranous and erythematous candidiasis (Lalla et al. 2010). There appear to be no relation to Candida colonization and the presence or severity of oral mucositis in haemopoietic progenitor cell transplant patients (Epstein et al. 2003; Westbrook et al. 2013), whereas C. glabrata has been associated with oral ulcerations in this patient group (Laheij et al. 2012). A recent study indicates that the mycobiome plays a role in the pathogenesis of acute graft-versus-host disease in blood- and marrow-transplanted patients (van der Velden et al. 2013).

Several studies have shown that the oral microbiota is disturbed in patients, who has received radiotherapy in the head and neck region, and in this regard found increased colonization of Candida species and higher occurrence of oral candidiasis (Al-Nawas and Grötz 2006; Almståhl and Wikström 2003; Almståhl et al. 2008; Brown et al. 1975; Grötz et al. 2003). C. albicans is the cause of the majority of oropharyngeal infections, but C. glabrata and C. tropicalis are emerging causes of these infections in patients with head and neck cancer. It has been shown that about 50 % of patients with head and neck cancer were colonized with Candida species prior to radiotherapy, and after the therapy the percentage has increased to about 75 % (Lalla et al. 2010). The increased colonization also translated into an increased rate of oral infections. Predisposing factors in patients with head and neck cancer include mucosal injury due to cancer therapy, salivary gland hypofunction, smoking and wearing dentures.