Mucosal Candidiasis
- Author: Crispian Scully, MD, PhD, MDS, CBE, MRCS, FDSRCS, FDSRCPS, FFDRCSI, FDSRCSE, FRCPath, FMedSci, FHEA, FUCL, DSc, DChD, DMed(HC), Dr(HC), ; Chief Editor: William D James, MD more...
Background
Candidosis (candidiasis) describes a group of yeastlike fungal infections involving the skin and mucous membranes. Infection is caused by Candida species, typically, Candida albicans. C albicans is ubiquitous and is found mainly on oral or genital mucosae; it may also be transmissible between consorts.[1]
Candidosis is seen orally in people with altered oral ecology (from dental appliances, hyposalivation, or the use of immunosuppressants or antimicrobials) and/or impaired immunity (eg, transplant recipients, persons on immunosuppressive treatments, persons with HIV/AIDS or other cellular immune defects).
By tradition, the most commonly used classification of oral candidosis divides the infection into 4 types including (1) acute pseudomembranous candidosis (thrush), (2) acute atrophic (erythematous) candidosis, (3) chronic hyperplastic candidosis, and (4) chronic atrophic (erythematous) candidosis.
Chronic hyperplastic candidosis was further subdivided into 4 groups based on localization patterns and endocrine involvement including (1) chronic oral candidosis (candidal leukoplakia), (2) endocrine candidosis syndrome, (3) chronic localized mucocutaneous candidosis, and (4) chronic diffuse candidosis.
Thrush (acute pseudomembranous candidosis) is the term used for the multiple white-fleck appearance of acute candid0sis, which purportedly resembles the appearance of the bird with the same name.
Erythematous candidosis is the term used for the red lesions of candidosis.
Pathophysiology
C albicans is the predominant causal organism of most candidosis. Other species, including Candida krusei, have appeared in persons who are severely immunocompromised. Candida glabrata is an emerging cause of oropharyngeal candidosis in patients receiving radiation for head and neck cancer.[2] In patients with HIV infection, new species, such as Candida dubliniensis and Candida inconspicua, have been recognized.
C albicans is a harmless commensal organism inhabiting the mouths of almost 50% of the population (carriers); persister cells are clinically relevant, and antimicrobial therapy selects for high-persister strains in vivo.[3]
Under certain circumstances, C albicans can become an opportunistic pathogen. Such a suitable circumstance for it to become an opportunist may be a disturbance in the oral flora or a decrease in immune defenses.
Acute pseudomembranous candidosis (thrush)
Thrush may be observed in healthy neonates or in persons in whom antibiotics, corticosteroids, or xerostomia disturb the oral microflora. Oropharyngeal thrush occasionally complicates the use of corticosteroid inhalers. Immune defects, especially HIV infection, immunosuppressive treatment, leukemias, lymphomas, cancer, and diabetes, may predispose patients to candidal infection.
Erythematous candidosis
Erythematous candidosis may cause a sore red mouth, especially of the tongue, in patients taking broad-spectrum antimicrobials. It also may be a feature of HIV disease. Median rhomboid glossitis is a red patch occurring in the middle of the dorsum in the posterior area of the anterior two thirds of the tongue and especially is observed in smokers and in those with HIV disease.
Chronic mucocutaneous candidosis
Chronic mucocutaneous candidosis (CMC) describes a group of rare syndromes, which sometimes include a definable immune defect, in which persistent mucocutaneous candidosis responds poorly to topical treatment. Generally, the more severe the candidosis, the greater the likelihood that immunologic defects (particularly of cell-mediated immunity) can be identified. Recent studies suggest a defect in cytokine (interleukin 2 and interferon-g) production in response to candidal and some bacterial antigens, with reduced TH1 lymphocyte function and enhanced TH2 activity (and increased interleukin 6), and reduced serum levels of immunoglobulin G2 and immunoglobulin G4.
Epidemiology
Frequency
United States
Candidosis is common in groups at risk, such as patients who are immunocompromised. Frequency of infection is rising, primarily because of HIV infection and both the increase in candidal species other than C albicans and the resistance to antifungals.
International
Candidosis is common in groups at risk, such as patients who are immunocompromised.
Mortality/Morbidity
Candidosis may predispose individuals to esophageal spread.
Sex
Candidosis is reported equally in males and females worldwide, except in areas where males with HIV infection outnumber females.
Age
Candidosis predominantly occurs in middle-aged or older persons; however, in those with HIV infection, candidal infection primarily occurs in the third and fourth decades.
Boriollo MF, Bassi RC, dos Santos Nascimento CM, Feliciano LM, Francisco SB, Barros LM. Distribution and hydrolytic enzyme characteristics of Candida albicans strains isolated from diabetic patients and their non-diabetic consorts. Oral Microbiol Immunol. Dec 2009;24(6):437-50. [Medline].
Redding SW, Dahiya MC, Kirkpatrick WR, et al. Candida glabrata is an emerging cause of oropharyngeal candidiasis in patients receiving radiation for head and neck cancer. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. Jan 2004;97(1):47-52. [Medline].
Lafleur MD, Qi Q, Lewis K. Patients with long-term oral carriage harbor high-persister mutants of Candida albicans. Antimicrob Agents Chemother. Jan 2010;54(1):39-44. [Medline].
Sitheeque MA, Samaranayake LP. Chronic hyperplastic candidosis/candidiasis (candidal leukoplakia). Crit Rev Oral Biol Med. 2003;14(4):253-67. [Medline].
Golecka M, Oldakowska-Jedynak U, Mierzwinska-Nastalska E, Adamczyk-Sosinska E. Candida-associated denture stomatitis in patients after immunosuppression therapy. Transplant Proc. Jan-Feb 2006;38(1):155-6. [Medline].
Tanida T, Okamoto T, Okamoto A, et al. Decreased excretion of antimicrobial proteins and peptides in saliva of patients with oral candidiasis. J Oral Pathol Med. Nov 2003;32(10):586-94. [Medline].
Niimi M, Firth NA, Cannon RD. Antifungal drug resistance of oral fungi. Odontology. Feb 2010;98(1):15-25.
Scardina GA, Ruggieri A, Messina P. Chronic hyperplastic candidosis: a pilot study of the efficacy of 0.18% isotretinoin. J Oral Sci. Sep 2009;51(3):407-10. [Medline].
Fanello S, Bouchara JP, Sauteron M, et al. Predictive value of oral colonization by Candida yeasts for the onset of a nosocomial infection in elderly hospitalized patients. J Med Microbiol. Feb 2006;55:223-8. [Medline].
Lynch DP. Oral candidiasis. History, classification, and clinical presentation. Oral Surg Oral Med Oral Pathol. Aug 1994;78(2):189-93. [Medline].
Rautemaa R, Hietanen J, Niissalo S, Pirinen S, Perheentupa J. Oral and oesophageal squamous cell carcinoma--a complication or component of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED, APS-I). Oral Oncol. Jul 2007;43(6):607-13. [Medline].
Scully C, el-Kabir M, Samaranayake LP. Candida and oral candidosis: a review. Crit Rev Oral Biol Med. 1994;5(2):125-57. [Medline].
Taillandier J, Esnault Y, Alemanni M. A comparison of fluconazole oral suspension and amphotericin B oral suspension in older patients with oropharyngeal candidosis. Multicentre Study Group. Age Ageing. Mar 2000;29(2):117-23. [Medline].

