Clinical oral Candida infection (candidiasis) is one of the common oral mucosal infections, and its management is usually frustrating due to either treatment failure or recurrence. Historically, oral candidiasis has been branded as disease of diseased. The unsuccessful management of oral candidiasis can due to either incorrect diagnosis, failure to identify (or correct) the underlying predisposing factor(s), or inaccurate prescription of antifungal agents. Failure to properly treat oral candidiasis will lead to persistence of the fungal cell in the oral cavity and hence recurrence of infection. The oral health care provider should be aware of these fall pits in order to successfully manage oral candidiasis. 1. Introduction Oral candidal colonization and candidiasis have recently received increased attention by the health care providers and researchers alike, particularly following the emergence of human immunodeficiency virus (HIV) infection and the widespread use of broad spectrum antibiotics and immunosuppressant therapy [1]. The genus Candida comprised more than 150 species which are widely spreading in the environment. Knowing that the majority of the species cannot live at the human body temperature [2] explains why the oral cavity is colonized with only a limited number of Candida species. Candida species constitute part of the oral harmless commensal flora in about 2–70% of the general population but is responsible for causing infection if the host immune barriers are breached either on the local or on the systemic level [1]. Candida albicans is the species largely responsible for oral candidiasis which is the most common human fungal infection especially in childhood and the elderly. It is not uncommon to encounter a recurrence of the oral candidal infection after some time of institution of antifungal therapy, which constitutes a frustration and disappointment for both the clinician and the patient. One study estimated that around 20% of patients with oral candidiasis experience infection recurrence and in around 30% of the recurrences the second isolate was different from that responsible for the first episode of infection [3]. This raises the question whether the “recurrence” is a second infection or due to “persistent” Candida cells. If the superficial oral candidal infection was not well managed in severe immunosuppression, the patient may become susceptible to esophageal spread of infection or to the potentially lethal systemic candidemia [4]. Therefore, it is essential for the oral candidal infection to be diagnosed accurately and managed
References
[1]
L. P. Samaranayake, “Oral mycoses in HIV infection,” Oral Surgery Oral Medicine and Oral Pathology, vol. 73, no. 2, pp. 171–180, 1992.
[2]
F. Schauer and R. Hanschke, “Taxonomy and ecology of the genus Candida,” Mycoses, vol. 42, no. S1, pp. 12–21, 1999.
[3]
F. Gallè, M. Sanguinetti, G. Colella et al., “Oral candidosis: characterization of a sample of recurrent infections and study of resistance determinants,” New Microbiologica, vol. 34, no. 4, pp. 379–389, 2011.
[4]
J. A. Vazquez, “Invasive fungal infections in the intensive care unit,” Seminars in Respiratory and Critical Care Medicine, vol. 31, no. 1, pp. 79–86, 2010.
[5]
D. W. Williams, R. P. C. Jordan, X. Q. We, et al., “Interactions of Candida albicans with host epithelial surfaces,” Journal of Oral Microbiology, vol. 5, pp. 224–234, 2013.
[6]
I. Olsen, “Oral adhesion of yeasts,” Acta Odontologica Scandinavica, vol. 48, no. 1, pp. 45–53, 1990.
[7]
S. W. Redding, M. C. Dahiya, W. R. Kirkpatrick et al., “Candida glabrata is an emerging cause of oropharyngeal candidiasis in patients receiving radiation for head and neck cancer,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, vol. 97, no. 1, pp. 47–52, 2004.
[8]
H. Egusa, N. S. Soysa, A. N. Ellepola, H. Yatani, and L. P. Samaranayake, “Oral candidosis in HIV-infected patients,” Current HIV Research, vol. 6, no. 6, pp. 485–499, 2008.
[9]
H. Terai and M. Shimahara, “Usefulness of culture test and direct examination for the diagnosis of oral atrophic candidiasis,” International Journal of Dermatology, vol. 48, no. 4, pp. 371–373, 2009.
[10]
R. Morgan, J. Tsang, N. Harrington, and L. Fook, “Survey of hospital doctors' attitudes and knowledge of oral conditions in older patients,” Postgraduate Medical Journal, vol. 77, no. 908, pp. 392–394, 2001.
[11]
J. Gibson, P.-J. Lamey, M. Lewis, and B. Frier, “Oral manifestations of previously undiagnosed non-insulin dependent diabetes mellitus,” Journal of Oral Pathology and Medicine, vol. 19, no. 6, pp. 284–287, 1990.
[12]
J. L. Rindum, A. Stenderup, and P. Holmstrup, “Identification of Candida albicans types related to healthy and pathological oral mucosa,” Journal of Oral Pathology and Medicine, vol. 23, no. 9, pp. 406–412, 1994.
[13]
G. R. Thompson III, P. K. Patel, W. R. Kirkpatrick et al., “Oropharyngeal candidiasis in the era of antiretroviral therapy,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, vol. 109, no. 4, pp. 488–495, 2010.
[14]
A. Sun, H.-P. Lin, Y.-P. Wang, and C.-P. Chiang, “Significant association of deficiency of hemoglobin, iron and vitamin B12, high homocysteine level, and gastric parietal cell antibody positivity with atrophic glossitis,” Journal of Oral Pathology & Medicine, vol. 41, no. 6, pp. 500–504, 2012.
[15]
H. Terai and M. Shimahara, “Atrophic tongue associated with Candida,” Journal of Oral Pathology and Medicine, vol. 34, no. 7, pp. 397–400, 2005.
[16]
S. Kiat-Amnuay and J. Bouquot, “Breastfeeding keratosis: this frictional keratosis of newborns may mimic thrush,” Pediatrics, vol. 132, no. 3, pp. e775–e778, 2013.
[17]
A. V. Abbeele, H. De Meel, M. Ahariz, J.-P. Perraudin, I. Beyer, and P. Courtois, “Denture contamination by yeasts in the elderly,” Gerodontology, vol. 25, no. 4, pp. 222–228, 2008.
[18]
Z. N. Al-Dwairi, “Prevalence and risk factors associated with denture-related stomatitis in healthy subjects attending a dental teaching hospital in North Jordan.,” Journal of the Irish Dental Association, vol. 54, no. 2, pp. 80–83, 2008.
[19]
L. Gendreau and Z. G. Loewy, “Epidemiology and etiology of denture stomatitis,” Journal of Prosthodontics, vol. 20, no. 4, pp. 251–260, 2011.
[20]
A. Y. Zhang, W. L. Camp, and B. E. Elewski, “Advances in topical and systemic antifungals,” Dermatologic Clinics, vol. 25, no. 2, pp. 165–183, 2007.
[21]
J. B. Epstein, E. L. Truelove, K. Hanson-Huggins et al., “Topical polyene antifungals in hematopoietic cell transplant patients: tolerability and efficacy,” Supportive Care in Cancer, vol. 12, no. 7, pp. 517–525, 2004.
[22]
J. W. Costerton, Z. Lewandowski, D. E. Caldwell, D. R. Korber, and H. M. Lappin-Scott, “Microbial biofilms,” Annual Review of Microbiology, vol. 49, pp. 711–745, 1995.
[23]
J. S. Finkel and A. P. Mitchell, “Genetic control of Candida albicans biofilm development,” Nature Reviews Microbiology, vol. 9, no. 2, pp. 109–118, 2011.
[24]
J. Nett, L. Lincoln, K. Marchillo et al., “Putative role of β-1,3 glucans in Candida albicans biofilm resistance,” Antimicrobial Agents and Chemotherapy, vol. 51, no. 2, pp. 510–520, 2007.
[25]
K. Lewis, “Persister cells,” Annual Review of Microbiology, vol. 64, pp. 357–372, 2010.
[26]
H. T. Taff, K. F. Mitchell, J. A. Edward, and D. R. Andes, “Mechanisms of Candida biofilm drug resistance,” Future Microbiology, vol. 8, no. 10, pp. 1325–1337, 2013.
[27]
I. L. Santana, L. M. Gon？alves, A. A. D. Vasconcellos, W. J. da Silva, J. A. Cury, and A. A. D. B. Cury, “Dietary carbohydrates modulate Candida albicans biofilm development on the denture surface,” PLoS ONE, vol. 8, no. 5, Article ID e64645, 2013.
[28]
J. E. Nett, K. Marchillo, C. A. Spiegel, and D. R. Andes, “Development and validation of an in vivo Candida albicans biofilm denture model,” Infection and Immunity, vol. 78, no. 9, pp. 3650–3659, 2010.
[29]
J. Chandra, P. K. Mukherjee, S. D. Leidich, et al., “Antifungal resistance of Candidal biofilms formed on denture acrylic in vitro,” Journal of Dental Research, vol. 80, no. 3, pp. 903–908, 2001.
[30]
R. Rautemaa and G. Ramage, “Oral candidosis—clinical challenges of a biofilm disease,” Critical Reviews in Microbiology, vol. 37, no. 4, pp. 328–336, 2011.
[31]
D. M. Kuhn and M. A. Ghannoum, “Candida biofilms: antifungal resistance and emerging therapeutic options,” Current Opinion in Investigational Drugs, vol. 5, no. 2, pp. 186–197, 2004.
[32]
S. Ganguly and A. P. Mitchell, “Mechanisms of Candida biofilm drug resistance. Mucosal biofilms of Candida albicans,” Current Opinion in Microbiology, vol. 14, pp. 380–385, 2011.
[33]
M. Ruhnke, “Epidemiology of Candida albicans infections and role of non-Candida-albicans yeasts,” Current Drug Targets, vol. 7, no. 4, pp. 495–504, 2006.
[34]
Y.-L. Yang and H.-J. Lo, “Mechanisms of antifungal agent resistance,” Journal of Microbiology, Immunology and Infection, vol. 34, no. 2, pp. 79–86, 2001.
[35]
A. M. Bal, “The echinocandins: three useful choices or three too many?” International Journal of Antimicrobial Agents, vol. 35, no. 1, pp. 13–18, 2010.
