Oral Candidiasis Is Primarily Caused by Candida Article Critique

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Oral candidiasis is primarily caused by Candida albicans, in which yeast adheres to the buccal epithelial cellular surface during the earliest phase of infection. This process is predominantly implicated by the hydrophobicity of fungus on the cell surface. The infection process is enabled by penetration of Candida albicans into the oral tissue, which is facilitated by secretion of exoenzymes and the development of hyphae (Calamari et al., 2011).

Following limited exposure to antifungal agents, growth recovery capacity can be measured through the post antifungal effect, which indicates virulence levels of yeast. Increasingly, there has been a demonstrated resistance to antifungals, which is a cause for concern since there are fewer antifungals available in comparison to antibiotics. Therefore, research has been directed toward investigations of alternatives to antifungals for the treatment of Candida albicans. A few of these alternatives include chlorhexidine-based oral rinses, fluconazole, and chitosan. The researchers in the study by Calamari et al. (2011) sought to investigate the antifungal and post anti-fungal effects of chlorhexidine, fluconazole, and chitosan individually and in combination, with regard to their effects on the virulence of Candida albicans.

In regards to the methods employed in this study, the first stage was the isolation and identification of ten isolated wild strains of Candida albicans (Calamari et al., 2011), which were isolated from the saliva of ten patients presenting with oral candidiasis, who were not under treatment with any sort of antifungal drug. The process used to identify the strains of Candida albicans involved germinative tube development test, assimilation of sugar and fermentation, and finally yeast growth within a chromogenic medium.

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In order to assess antifungal effects, chlorhexidine solutions, fluconazole, and chitosan and their combinations were used in phosphate saline buffer, and minimum inhibitory concentration was determined. This minimum inhibitory concentration was essentially the lowest concentration of antifungal agent that results in considerable colony size decrease in comparison to growth of controls. Also, germinative tube development was induced, and both cell surface hydrophobicity and post antifungal effect were determined. Moreover, all experiments in the study were done three times, and the data involved were analyzed through the use of Spearman's correlation coefficient, Student's t-test for independent samples with a significance level of p

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