Oral bacteria modulate Candida biofilm formation

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Candida krusei infections and fluconazole therapy

Candida species are by far the most common agents of mucosal fungal infection in man. While Candida albicans is the most notorious pathogen in this group, non-albicans species such as Candida krusei are gradually emerging as pathogens of concern, especially in compromised hosts. It is thought that the wide use of the newer triazole drug, fluconazole, in HIV- infected individuals is contributing to this phenomenon. Studies in both humans and animals have now demonstrated prophylactic and therapeutic failure of fluconazole against C. krusei due to increasing resistance of the organism to this azole. Thus, the indiscriminate use of fluconazole, a drug with relatively minimal toxicity and excellent pharmacokinetics, may lead to the development of widespread resistance to this azole among Candida species.published_or_final_versio

Turbidometric evaluation of polyene-azole antagonism in C. albicans

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Correlation between the cyclin A and p53 gene expression in oral carcinogenesis

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Oral Candida infections--a review.

Candida species are the commonest agents of oral mycoses. They cause a variety of diseases including the new variant, erythematous candidosis, which is frequently described in HIV infection. Due to these and other reasons the classification of oral candidosis has been recently revised, and further more new therapeutic regimes have been described. Hence in this article an overview of oral Candida infections is presented with special emphasis on current concepts related to classification and treatment.published_or_final_versio

Studies on the susceptibility of Candida species to lactoferrin

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Proteinase production by Candida albicans in HIV infection and its attenuation by antimycotics

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Human Serum Promotes Candida albicans Biofilm growth and Virulence Gene Expression on Silicone Biomaterial

Objectives Systemic candidal infections are a common problem in hospitalized patients due to central venous catheters fabricated using silicone biomaterial (SB). We therefore evaluated the effect of human serum on C. albicans biofilm morphology, growth, and the expression of virulence-related genes on SB in vitro. Methods We cultivated C. albicans SC5314 (wild-type strain, WT) and its derivative HLC54 (hyphal mutant, HM) for 48 h in various conditions, including the presence or absence of SB discs, and human serum. The growth of planktonic and biofilm cells of both strains was monitored at three time points by a tetrazolium salt reduction assay and by scanning electron microscopy. We also analyzed by RT-PCR its expression of the virulence-related genes ALS3, HWP1, EAP1, ECE1, SAP1 - SAP10, PLB1, PLB2, PLC and PLD. Results At each time point, planktonic cells of WT strain cultured in yeast nitrogen base displayed a much higher expression of EAP1 and HWP1, and a moderately higher ALS3 expression, than HM cells. In planktonic cells, expression of the ten SAP genes was higher in the WT strain initially, but were highly expressed in the HM strain by 48 h. Biofilm growth of both strains on SB was promoted in the presence of human serum than in its absence. Significant upregulation of ALS3, HWP1, EAP1, ECE1, SAP1, SAP4, SAP6 - SAP10, PLB1, PLB2 and PLC was observed for WT biofilms grown on serum-treated SB discs for at least one time point, compared with biofilms on serum-free SB discs. Conclusions Human serum stimulates C. albicans biofilm growth on SB discs and upregulates the expression of virulence genes, particularly adhesion genes ALS3 and HWP1, and hydrolase-encoding genes SAP, PLB1 and PLB2. This response is likely to promote the colonization of this versatile pathogen within the human host.published_or_final_versio

Chronic hyperplastic candidosis/candidiasis (candidal leukoplakia)

Chronic hyperplastic candidosis/candidiasis (CHC; syn. candidal leukoplakia) is a variant of oral candidosis that typically presents as a white patch on the commissures of the oral mucosa. The major etiologic agent of the disease is the oral fungal pathogen Candida predominantly belonging to Candida albicans, although other systemic co-factors, such as vitamin deficiency and generalized immune suppression, may play a contributory role. Clinically, the lesions are symptomless and regress after appropriate antifungal therapy and correction of underlying nutritional or other deficiencies. If the lesions are untreated, a minor proportion may demonstrate dysplasia and develop into carcinomas. This review outlines the demographic features, etiopathogenesis, immunological features, histopathology, and the role of Candida in the disease process. In the final part of the review, newer molecular biological aspects of the disease are considered together with the management protocols that are currently available, and directions for future research.published_or_final_versio

Salivary immunoglobulin A levels in "rapid" and "slow" plaque formers

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