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Structure and Physiology
Candida albicans is a diploid, Gram-positive fungus that can take on a unicellular (yeast) or multicellular (hyphae, pseudohyphae) form. A unique characteristic to this microbe is that it can switch between different phenotypes. The change between the two phenotypes can happen multiple times and is spontaneous. Studies show strong evidence that these phenotype switches are due to the change in the control of regulatory gene expression. One phenotype of this microbe is white, round cells in smooth colonies. The other phenotypic form is opaque, rod-shaped in flat, gray colonies. The two forms have different antigen expression and different affinities for tissues. This evolutionary advantage allows it to be highly adaptive to environmental changes.
Transmission and Disease
Humans normally share a commensalism relationship with C. albicans, but C. albicans can become pathogenic if a person is immunocompromised or if there is a change in their normal microbiota. C. albicans prefers to invade the skin or mucosae but can also infect the blood, heart, and lungs.
Candida albicans can survive for long periods of time without nutrients and is known to form biofilms on medical devices; therefore, disinfection to kill these fungi is very important.
C. albicans has been shown to encode the standard Leucine (CUG) codon as serine. As a divergence from the standard genetic code, it is thought to have given the organism an evolutionary advantage driven by selection.
- Holland LM, Schröder MS, Turner SA, Taff H, Andes D, Grózer Z, Gácser A, Ames L, Haynes K, Higgins DG, Butler G. Comparative Phenotypic Analysis of the Major Fungal Pathogens Candida parapsilosis and Candida albicans. PLoS Pathog. 2014 Sep 18;10(9):e1004365. doi: 10.1371/journal.ppat.1004365. eCollection 2014.
- Santos, MA; Cheesman, C; Costa, V; Moradas-Ferreira, P; Tuite, MF (February 1999). "Selective advantages created by codon ambiguity allowed for the evolution of an alternative genetic code in Candida spp.". Molecular Microbiology 31 (3): 937–947. doi:10.1046/j.1365-2958.1999.01233.x. PMID 10048036.