Rapid and accurate identification of Candida species is critical for guiding antifungal therapy, especially with the emergence of intrinsically resistant pathogens. However, diagnostics using culture-based methods remain slow and labor-intensive, limiting timely treatment decisions. This systematic review evaluated the diagnostic performance and clinical applicability of nucleic acid amplification tests (NAATs) for Candida species identification using a PubMed search completed on 23 June 2025. A total of 888 records were screened, 333 full-text articles were assessed, and 158 studies were included based on criteria including comparison with standard diagnostic methods, diagnostic performance reporting, and involvement of clinical samples. PCR-based approaches were the most widely used, including conventional, nested, multiplex, real-time, and droplet digital PCR. Isothermal methods such as loop-mediated isothermal amplification (LAMP) and recombinase polymerase amplification (RPA) were increasingly represented. Common molecular targets included the ITS and 18S/28S rDNA regions. The risk of bias assessment was completed with the QUADAS-2 tool. Diagnostic performance varied depending on assay design, specimen type, gene target, and reference method. Excellent specificity and low limits of detection were achieved, especially with isothermal platforms offering the shortest turnaround times and greatest potential for point-of-care implementation. Multiplex assays were particularly advantageous for detecting mixed-species samples, while highly specific assays were optimal for distinguishing clinically important species such as Candidozyma auris, Nakaseomyces glabratus, and Pichia kudriavzevii. Overall, NAATs represent a promising diagnostic tool for Candida species identification, but broader clinical adoption will require improved standardization, validation across diverse patient populations, and clearer interpretation of fungal burden in the context of colonization versus infection.

Candida auris is a multidrug-resistant fungal pathogen for which echinocandins are recommended first-line therapy, yet its adaptive responses to this drug class remain incompletely understood. This study defined the genome-wide transcriptional responses of C. auris strain B11244 (Clade IV) to subinhibitory caspofungin, micafungin, and anidulafungin and examined whether shared responses corresponded to cell-wall remodeling. Growth-based broth microdilution indicated susceptibility to all three drugs by MIC (caspofungin, approximately 0.5–1 µg/mL; micafungin, 0.125 µg/mL; anidulafungin, approximately 0.03125 µg/mL), but caspofungin uniquely produced marked paradoxical growth at 4–8 µg/mL, consistent with caspofungin tolerance. RNA sequencing identified 2920, 2130, and 2149 differentially expressed genes following caspofungin, micafungin, and anidulafungin exposure, respectively, including 283 co-upregulated and 157 co-downregulated genes. All three drugs induced a conserved cell-wall integrity program marked by transcriptional induction of Bck1-Mkc1 and Hog1 MAPK pathway components and an 18-gene signature involved in chitin synthesis and cell-wall cross-linking. The response was strongest with caspofungin, and RT-qPCR corroborated representative transcriptional changes. No canonical FKS1 hotspot mutation was detected; an I1572L substitution was predicted to be structurally neutral. Calcofluor White microscopy showed qualitatively enhanced peripheral fluorescence following each treatment, whereas colorimetric glucosamine measurement demonstrated significantly increased bulk chitin only with caspofungin (149% of control); micafungin (120%) and anidulafungin (98%) did not differ significantly from control. Taken together, these findings are consistent with inducible, MAPK-associated cell-wall remodeling as a potential FKS1-independent contributor to echinocandin tolerance, while showing that transcriptional convergence does not imply uniform phenotypic outcomes.