Pathogenesis of Candida infections - 12/10/17
Abstract |
Candida infections of the skin and superficial mucosal sites are the result of an interplay between fungal virulence and host defenses. Epidermal proliferation and T-lymphocyte immune responses are expressed by the host to combat fungal invasion, but inflammatory responses and nonspecific inhibitors also probably play a role. Candida albicans can express at least three types of surface adhesion molecules to colonize epithelial surfaces, plus an aspartyl proteinase enzyme able to facilitate initial penetration of keratinized cells. Deeper penetration of keratinized epithelia is assisted by hypha formation, and C. albicans hyphae may use contact sensing (thigmotropism) as a guiding mechanism. Pathogenesis requires differential expression of virulence factors at each new stage of the process: a propensity for rapid alteration of the expressed phenotype in C. albicans may therefore be a significant factor in establishing the comparatively high pathogenic potential of this species.
Le texte complet de cet article est disponible en PDF.† | Presented at the “International Summit on Cutaneous Antifungal Therapy,” Supported by educational grants from janssen pharmaceutica; Ortho Pharmaceutical Corporation–Dermatological division; Roerig–A division of pfizer; and sandoz pharmaceuticals corporation. |
Vol 31 - N° 3P2
P. S2-S5 - septembre 1994 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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