The genus Candida encompasses diverse yeasts that cause infections in humans, collectively termed candidiasis. For decades, Candida albicans has been the most frequently isolated fungal pathogen, responsible for infections ranging from mucosal thrush to life-threatening bloodstream infections. The landscape of fungal threats shifted dramatically with the emergence of Candida auris, first identified in 2009. C. auris has rapidly become a global public health concern due to its high transmissibility within healthcare settings and its frequent resistance to multiple classes of antifungal medications. This comparison details the distinct characteristics of C. albicans and C. auris, revealing why one is a persistent medical challenge and the other represents a new, urgent threat.
Structural and Growth Differences
The physical structures and growth patterns of the two species reflect their distinct survival strategies. C. albicans exhibits dimorphism, switching between a yeast form and a filamentous form consisting of pseudohyphae and true hyphae. This morphological plasticity is a major factor in its virulence; the yeast form facilitates bloodstream dissemination while the hyphal form allows for tissue invasion. C. albicans forms robust biofilms on medical devices, creating a protective matrix that shields the cells from the host immune system and antifungal drugs.
In contrast, C. auris primarily grows as a budding yeast. It rarely forms true hyphae, though some strains can develop pseudohyphae-like forms under stress conditions. C. auris forms a distinct, sticky biofilm that plays a key role in its ability to persist and spread on surfaces within hospitals. Unlike C. albicans, which is a commensal organism often residing in the human gastrointestinal tract, C. auris is not typically part of the normal human microflora, instead colonizing the skin.
Genomic and Evolutionary Distinction
The underlying genetic architecture of these two species contributes significantly to their different adaptive capacities. C. albicans is typically a heterozygous diploid organism, possessing two sets of chromosomes. This diploid nature provides genetic buffering, where a harmful mutation on one chromosome may be masked by the functional copy on the homologous chromosome. C. albicans also exhibits high genomic plasticity, frequently undergoing events like loss of heterozygosity, which can rapidly alter its phenotype, contributing to its adaptability in diverse host niches.
C. auris generally presents as a haploid organism, possessing only one set of chromosomes. Because of this haploid state, a single recessive mutation can be immediately expressed, potentially allowing for faster adaptation to environmental pressures, such as antifungal exposure. A defining feature of C. auris is its division into five major, geographically distinct clades. High frequency of aneuploidy, or having an abnormal number of chromosomes, is also a significant mechanism in C. auris that allows for rapid adaptation, particularly in response to antifungal treatment.
Comparing Antifungal Drug Susceptibility
The most significant difference between the two species lies in their response to antifungal medications. C. albicans is generally susceptible to all three major classes of antifungals: azoles, echinocandins, and polyenes. When resistance occurs in C. albicans, it is typically acquired during treatment through mechanisms such as the overexpression of drug efflux pumps or point mutations in target enzyme genes, particularly the ERG11 gene for azole resistance.
In stark contrast, C. auris is characterized by its high frequency of inherent, simultaneous multidrug resistance (MDR), which is the primary reason for global concern. Resistance to azole-class drugs, such as fluconazole, is widespread, approaching 90% in many isolates in the United States. This high resistance is often linked to specific mutations in the ERG11 gene and the overexpression of drug transporter genes.
Echinocandins are often considered a first-line treatment for C. auris infections, and resistance rates are generally low. However, resistance to echinocandins can rapidly develop during patient treatment, frequently involving mutations in the FKS1 gene. Polyenes, such as amphotericin B, remain broadly effective against C. auris, but resistance is emerging, with up to 30% of isolates showing resistance in some regions. The emergence of pan-drug-resistant C. auris isolates, resistant to all three major drug classes, highlights the severity of the treatment challenge and necessitates alternative or combination therapies.