Mucosal Candidiasis

Mucosal Candidiasis

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Candidiasis describes a group of fungal infections involving the skin and mucous membranes. Infection is caused by Candida species, primarily Candida albicans. [1] C albicans is a dimorphic fungus that can asymptomatically colonize the oral or genital mucosae in healthy individuals. [2] Oral colonization is estimated in 50% of healthy adults, [3] while genital colonization is seen in 21% of women. [4] When the local ecology is disturbed, or where there is an immune defect, Candida overgrowth may lead to an opportunistic infection. The mucosal surfaces primarily affected by candidiasis are the oral cavity, esophagus, angles of the mouth, and genitals (causing vulvovaginitis in females, balanitis in males).

Oral candidiasis may present as either white or erythematous lesions and either an acute or chronic infection. [5] Thus, the presentations can be divided into the following four subtypes:

There are also conditions that may predispose individuals to chronic, multifocal infections from Candida. This can lead to syndromes such as chronic mucocutaneous candidiasis (CMC).

C albicans is a dimorphic fungus that asymptomatically inhabits the mouths of almost 50% of the population. Overgrowth of Candida is protected against by local T cells and interleukin (IL)–17. [6] Thus, when immunity is compromised, growth proceeds unchecked and leads to opportunistic infections.

Candidiasis is seen in people with altered ecology, which in oral cases can be attributed to dental appliances, xerostomia, antimicrobials, nasopharyngeal steroids, or oral cancer. Impaired systemic immunity is another major cause of infection, notably in patients who are on immunosuppressive therapy, infected by HIV, or have diabetes. [7, 8]

C albicans is the predominant causal organism of most candidiasis. Other species, such as Candidatropicalis and Candidastellatoidea, more often appear in persons who are severely immunocompromised.

Secreted aspartyl proteinases (SAPs) are proteins secreted by Candida that contribute to virulence by facilitating invasion and inflammation. The prevacuolar protein sorting gene, VPS4, is required for extracellular secretion of SAPs, and it is a key component of the virulence of Candida. [9] Additionally, studies have shown that women with vulvovaginal candidiasis have higher levels of SAPs in their vaginal fluid. [10]

In those with dental devices, Candida, upon attachment, can form a small subcolony of persister cells. These cells have been shown to be highly resistant to antimicrobials, and they provide a mechanism for the recurrent formation of biofilms. [11]

Chronic mucocutaneous candidiasis (CMC) describes a group of rare syndromes, in which persistent mucocutaneous candidiasis responds poorly to topical treatment. It is associated with immune defects, particularly in T-cell, dendritic cell, and T-helper 17 (Th17) cell function. Studies have demonstrated specific signals that when compromised, cause defects in the response to candidal antigens. Identified defects include overproduction of IL-6, underproduction of IL-23, and deficiency of IL-17.

There are many risk factors that increase the incidence of candidiasis. Immunosuppression is the most significant of these, and it can be due to diabetes, antibiotics, immunosuppression, systemic steroid use, and HIV infection, among others.

The prognosis is good for most infections in the immunocompetent host, but in patients who are immunocompromised, antifungal resistance is commonplace. Oral candidiasis may predispose individuals to esophageal spread. Systemic spread is rare, but can occur in the severely immunocompromised.

For patient education resources, see the following:

Stoopler ET, Sollecito TP. Oral mucosal diseases: evaluation and management. Med Clin North Am. 2014 Nov. 98 (6):1323-52. [Medline].

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. 2009 Dec. 24(6):437-50. [Medline].

Arendorf TM, Walker DM. The prevalence and intra-oral distribution of Candida albicans in man. Arch Oral Biol. 1980. 25 (1):1-10. [Medline].

Pirotta MV, Garland SM. Genital Candida species detected in samples from women in Melbourne, Australia, before and after treatment with antibiotics. J Clin Microbiol. 2006 Sep. 44 (9):3213-7. [Medline].

Millsop JW, Fazel N. Oral candidiasis. Clin Dermatol. 2016 Jul-Aug. 34 (4):487-94. [Medline].

Conti HR, Peterson AC, Brane L, Huppler AR, Hernández-Santos N, Whibley N, et al. Oral-resident natural Th17 cells and γδ T cells control opportunistic Candida albicans infections. J Exp Med. 2014 Sep 22. 211 (10):2075-84. [Medline].

Meighani G, Aghamohammadi A, Javanbakht H, Abolhassani H, Nikayin S, Jafari SM, et al. Oral and dental health status in patients with primary antibody deficiencies. Iran J Allergy Asthma Immunol. 2011 Dec. 10(4):289-93. [Medline].

Alnuaimi AD, Wiesenfeld D, O’Brien-Simpson NM, Reynolds EC, McCullough MJ. Oral Candida colonization in oral cancer patients and its relationship with traditional risk factors of oral cancer: a matched case-control study. Oral Oncol. 2015 Feb. 51 (2):139-45. [Medline].

Rane HS, Hardison S, Botelho C, Bernardo SM, Wormley F Jr, Lee SA. Candida albicans VPS4 contributes differentially to epithelial and mucosal pathogenesis. Virulence. 2014. 5 (8):810-8. [Medline].

Cassone A. Vulvovaginal Candida albicans infections: pathogenesis, immunity and vaccine prospects. BJOG. 2015 May. 122 (6):785-94. [Medline].

Lafleur MD, Qi Q, Lewis K. Patients with long-term oral carriage harbor high-persister mutants of Candida albicans. Antimicrob Agents Chemother. 2010 Jan. 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].

Lalla RV, Patton LL, Dongari-Bagtzoglou A. Oral candidiasis: pathogenesis, clinical presentation, diagnosis and treatment strategies. J Calif Dent Assoc. 2013 Apr. 41 (4):263-8. [Medline].

[Guideline] Pappas PG, Kauffman CA, Andes DR, Clancy CJ, Marr KA, Ostrosky-Zeichner L, et al. Executive Summary: Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2016 Feb 15. 62 (4):409-17. [Medline].

Karbach J, Ebenezer S, Warnke PH, Behrens E, Al-Nawas B. Antimicrobial effect of Australian antibacterial essential oils as alternative to common antiseptic solutions against clinically relevant oral pathogens. Clin Lab. 2015. 61 (1-2):61-8. [Medline].

De Seta F, Schmidt M, Vu B, Essmann M, Larsen B. Antifungal mechanisms supporting boric acid therapy of Candida vaginitis. J Antimicrob Chemother. 2009 Feb. 63 (2):325-36. [Medline].

Centers for Disease Control and Prevention. Vulvovaginal Candidiasis. Available at https://www.cdc.gov/std/tg2015/candidiasis.htm. June 4, 2015; Accessed: August 28, 2017.

Niimi M, Firth NA, Cannon RD. Antifungal drug resistance of oral fungi. Odontology. 2010 Feb. 98 (1):15-25. [Medline].

Finch RG, Greenwood D, Whitley RJ, Norrby SR. Superficial and mucocutaneous mycoses. Antibiotic and Chemotherapy. 9th ed. Philadelphia, Pa: Elsevier Saunders; 2010.

Bolognia J, Jorizzo JL, Schaffer JV. Infections, infestations and bites. Dermatology. 3rd ed. Philadelphia, Pa: Elsevier Saunders; 2012. Sect. 12.

Surbhi Gupta University of Virginia School of Medicine

Surbhi Gupta is a member of the following medical societies: American Medical Association, American Medical Student Association/Foundation

Disclosure: Nothing to disclose.

Barbara B Wilson, MD Edward P Cawley Associate Professor, Department of Dermatology, University of Virginia School of Medicine

Barbara B Wilson, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Medical Society of Virginia, Sigma Xi

Disclosure: Nothing to disclose.

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.

Franklin Flowers, MD Department of Dermatology, Professor Emeritus Affiliate Associate Professor of Pathology, University of Florida College of Medicine

Franklin Flowers, MD is a member of the following medical societies: American College of Mohs Surgery

Disclosure: Nothing to disclose.

Mucosal Candidiasis

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