Candida albicans is a normal part of the human commensal flora, however it is also one of the most common fungal species that can cause human disease. It has recently become the fourth highest cause of nosocomial (hospital-acquired) sepsis, which carries a mortality rate of approximately 40%.
C. albicans causes multiple types of infections but they can be broadly divided into two groups: mucosal and systemic. Mucosal infections present commonly in otherwise healthy women as vulvovaginal candidiasis (thrush), which up to 75% adult women will experience at least once in their life time. C. albicans can also colonise the mouth (oral candidiasis) and can be a problem in newborns and the elderly.
Systemic infection, or disseminated candidiasis, is a much more serious disease. This occurs when a patient is immunosuppressed (due to drugs, chemotherapy or HIV) and C. albicans, normally kept under control by the immune system, invades tissues and enters the bloodstream. C. albicans commonly lives in the human gut therefore invasion of the gut wall by C. albicans (for example, through an ulcer or wound) is thought to be a common way in which disseminated candidiasis can start.
C. albicans morphological forms
C. albicans has three distinct morphological forms. It forms:
- a budding yeast,
- pseudohyphae ,and
- filamentous hyphae (Figure 1).
The ability to switch between these forms is dependent on a number of environmental factors and is essential for this fungus to be virulent. Mutant strains locked into just one of these morphologies have a decreased capacity to infect mice.
Figure 1. The three morphological forms of Candida albicans. Yeast (1) are small, round cells that divide by conventional cell division. True hyphae (3) are elongated cells that do not separate following cell division and are separated by specialised septa that allow passage of cytoplasm and other components between compartments. Pseudohyphae (2) are less elongated hyphae which are more constricted at septa than true hyphae. Pictures courtesy of Simon Vautier.
Immunity to C. albicans
A crucial component in the defence against C. albicans is the pattern recognition receptor, Dectin-1. Dectin-1 is expressed by innate myeloid cells such as monocytes, dendritic cells and neutrophils. Dectin-1 is required for the efficient phagocytosis and killing of C. albicans, because it binds β-glucans which form a layer within the C. albicans cell wall. Mice deficient in Dectin-1 are highly susceptible to disseminated candidiasis. Likewise, humans with the Dectin-1 polymorphism, Y238X, are much more likely to suffer from recurrent C. albicans infections.
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