Candida species are ubiquitous commensal yeast that usually reside as part of an individual´s normal mucosal microflora and can be detected in approximately 50% of the population in this form. However, if the balance of the normal flora is disrupted or the immune defences are compromised,
Candida species can invade mucosal surfaces and cause disease manifestations. Determining exactly how this transformation from commensal to pathogen takes place and how it can be prevented is a continuing challenger for the medical mycology field. Attributes that contribute to
Candida albicans
virulence include adhesion, hyphal formation, phenotypic switching and extra cellular hydrolytic enzyme production. The extra cellular hydrolytic enzyme, especially the secreted aspartyl proteinases (Saps), are one a few gene products that have been shown to directly contribute to
C. albicans pathogenicity. Given the limited number of suitable and effective antifungal drugs, the continuing increase in the incidence of
Candida infections, together with increasing drug resistance, highlights the need to discover new and better agents that target fundamental biological processes and or pathogenic determinants of
C. albicans.
