Antifungal resistance and susceptibility

CanID-PCR is a low-cost PCR tool that rapidly identifies Candida species from blood culture bottles with 97% accuracy compared to standard microbiology lab methods.

This study identifies Penicillium species contaminating cadavers and finds they are resistant to cold and ethanol, but susceptible to common disinfectants.

This study shows that Candida albicans and Enterococcus faecalis synergistically increase host cell damage through physical interaction and glucose depletion.

This study compares antifungal susceptibility of clinical and environmental Scedosporium and Lomentospora isolates from Taiwan, finding olorofim has consistently low MICs while triazoles show species-specific activity.

This study investigates the synergistic antifungal effects of curcumin nanosuspension and fluconazole against azole-resistant Candida albicans, showing improved bioavailability and biofilm disruption.

This study shows mucoricin disrupts neutrophil swarming by binding β-glucan, promoting mucormycosis, and identifies therapeutic strategies to counteract this effect.

This study characterizes the phenotypic and genomic diversity of Candida dubliniensis isolates from HIV-positive individuals, revealing significant variability in drug resistance and other clinically relevant traits.

This paper introduces a novel in vitro method to assess antifungal synergy and antagonism in C. albicans isolates, showing isolate-specific interaction patterns across three antifungals.

This study uses single-cell RNA sequencing to analyze human airway epithelial cell responses to Aspergillus and Coccidioides, revealing distinct stress and cytokine pathways.

This study shows that iron binding to caspofungin reduces its antifungal efficacy against Candida albicans and other fungi in iron-overloaded conditions.

This study identifies Mrr1 as a transcription factor coordinating MDR1 and CDR1 expression in Candida lusitaniae, contributing to antifungal resistance through efflux pumps and stress response genes.

This study identifies Tsa1b as a virulence factor in Candida auris that enhances oxidative stress resistance and infection progression.

This study shows that combining azole antifungals with different Cyp51 isozyme selectivities synergistically inhibits fungi with multiple Cyp51 isozymes.

This study shows that plasma gelsolin reduces inflammation and fungal burden in a mouse model of candidemia, enhancing innate immune function.

This paper describes a clinical case of acquired amphotericin B resistance in Candidozyma auris due to a frameshift mutation in ERG3, showing a fitness cost associated with altered sterol production.

The paper shows that inhibiting translation initiation helicases with Rocaglamide A increases yeast susceptibility to caspofungin, suggesting combination therapy could reduce resistance.

This study analyzes C. albicans biofilm formation using multiscale fluorescence microscopy and introduces new quantification methods to understand growth dynamics and environmental influences.

The paper investigates how Erg3 loss-of-function contributes to echinocandin resistance in Candida species by analyzing combined mutations in ERG3 and FKS2.

The paper identifies ergosterol depletion in Nakaseomyces glabratus as a mechanism for amphotericin B resistance without fitness or virulence defects.

This paper identifies 4456dh, a small molecule inhibitor of trehalose-6-phosphate synthase, which disrupts fungal thermal tolerance and virulence.

This study shows that co-culturing Candida albicans and Staphylococcus aureus increases secretion of virulence factors from both species, with C. albicans Als1p/Als3p playing a key role in this effect.

This study identifies CaFun30 as a potential antifungal target by screening a small molecule library and validating F1853-0039 as a lead inhibitor against C. albicans.

This study shows that FKS1-S639 mutations confer caspofungin resistance in C. auris but cause moderate fitness trade-offs without reducing virulence.

This study identifies over 20 drugs that induce echinocandin tolerance in Candida albicans, revealing their mechanism involves multiple signaling pathways and transcriptional changes.

The paper curates AMR mutations in fungi to create FungAMR, identifies universal resistance mutations, and provides a tool to screen genomes for AMR mutations.

This study shows that sub-inhibitory azole exposure enhances Candida glabrata virulence by upregulating yapsin proteases and altering host-pathogen interactions.

The paper tracks the development of multi-drug resistance in Candida auris isolates from a patient during antifungal treatment, identifying genetic mutations linked to resistance.

This study identifies the calcineurin pathway's role in regulating thermotolerance, cell integrity, antifungal resistance, and virulence in Candida auris through genetic deletion and transcription factor analysis.

This study identifies 34 drugs that affect antifungal efficacy in Candida albicans, with some promoting resistance when combined with fluconazole.