The Candida albicans is one of the most important global opportunistic pathogens, and the incidence of candidiasis has increased over the past few decades. Despite the established role of skin in defense against fungal invasion, little has been documented about the pathogenesis of Candida species when changing from normal flora to pathogens of vaginal and gastrointestinal epithelia. This study was carried out to determine in vivo and in vitro pathogenesis of clinical C. albicans strains isolated from skin lesions
In this study, association of in vivo and in vitro pathogenesis of C. albicans isolates with different evolutionary origins was investigated. Oral and systemic experimental candidiasis was established in BALB/C mice. The expression levels of secreted aspartyl proteinases (SAP1-3 genes), morphological transformation, and biofilm-forming ability of C. albicans were evaluated.
All the strains showed in vitro and in vivo pathogenicity by various extents. The SAP1, SAP2 and SAP3 genes were expressed in 50%, 100%, and 75% of the strains, respectively. The biofilm formation ability was negative in 12% of the strains, while it was considerable in 38% of the strains. Fifty percent of the strains had no phospholipase activity, and no one demonstrated high level of this pathogenesis factor. Relatively all the strains had very low potency to form pseudohyphae.
Our findings demonstrated that Candida albicans strains isolated from cutaneous candidiasis were able to cause oral and systemic infections in mice, so they could be considered as the potential agents of life-threatening nosocomial candidiasis in susceptible population.
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