Research Topic: drug resistance mechanisms

Ploidy plasticity drives fungal resistance to azoles used in agriculture and clinics

Agricultural fungicides called azoles can cause fungi to change their genetic makeup in ways that make them resistant to medical antifungal drugs. Researchers found that when Candida tropicalis (a fungal pathogen) is exposed to tebuconazole, an agricultural fungicide, it can transform into a haploid form (with half the normal chromosomes) that is resistant to both agricultural and clinical azoles. This discovery helps explain why fungal infections are becoming harder to treat in hospitals.

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Overexpression of efflux pump and biofilm associated genes in itraconazole resistant Candida albicans isolates causing onychomycosis

This research examines why some fungal infections of the nails resist treatment with the antifungal drug itraconazole. Scientists found that resistant fungi produce more proteins that pump the drug out of their cells (efflux pumps) and form protective biofilm structures. Understanding these resistance mechanisms could help develop better combination treatments that work alongside antifungal drugs to overcome resistance.

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Emerging antifungal resistance in Trichophyton mentagrophytes: insights from susceptibility profiling and genetic mutation analysis

This study examined how common skin fungal infections caused by Trichophyton species are becoming resistant to standard antifungal treatments. Researchers tested 131 fungal isolates from China and analyzed their resistance genes to understand why some strains no longer respond to terbinafine and other antifungal drugs. They found that certain genetic mutations, particularly in the SQLE gene, make these fungi resistant to treatment and that different species have different resistance patterns. These findings help doctors better choose treatments and guide the development of new antifungal medications.

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Metabolic Patterns of Fluconazole Resistant and Susceptible Candida auris Clade V and I

Researchers used advanced chemical analysis to identify different compounds produced by a dangerous fungus called Candida auris that can cause serious infections. They compared fungal strains that were resistant to the antifungal drug fluconazole with those that were susceptible, finding that resistant strains produced different metabolites (chemical compounds) than susceptible ones. These findings could help doctors develop better treatments by identifying what makes this fungus resistant to current medications.

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Analysis of Susceptibility and Drug Resistance of Antifungal Agents in Aspergillosis and Mucormycosis Patients: A Systematic Review

This comprehensive study analyzed how well five major antifungal drugs work against common disease-causing fungi like Aspergillus and Mucorales. Researchers reviewed 96 studies examining over 16,000 fungal samples to understand resistance patterns. The findings show that different fungi respond better to different drugs—for example, Aspergillus flavus responds well to voriconazole, while amphotericin B works best against other Aspergillus species. This information helps doctors choose the most effective treatments for fungal infections in vulnerable patients.

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Leveraging synthetic genetic array screening to identify therapeutic targets and inhibitors for combatting azole resistance in Candida glabrata

Candida glabrata is a dangerous fungus causing serious infections that is becoming resistant to antifungal drugs. Researchers used a genetic screening technique to find genes that interact with drug resistance mutations and identified methotrexate (a drug already used for arthritis) as a potential partner for fluconazole treatment. When combined, these drugs work better together against resistant strains of the fungus, offering hope for treating these stubborn infections.

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Loss of the Aspergillus fumigatus spindle assembly checkpoint components, SldA or SldB, generates triazole heteroresistant conidial populations

This research reveals that disabling certain cell division checkpoint proteins in the fungus Aspergillus fumigatus creates populations resistant to triazole antifungal drugs. The resistant fungal cells appear to have abnormal amounts of genetic material, suggesting that loss of these checkpoint controls allows cells with extra chromosomes to survive drug exposure. This discovery provides new insight into how dangerous fungal infections can develop resistance to our most important antifungal treatments.

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Ploidy plasticity drives fungal resistance to azoles used in agriculture and clinics

Agricultural fungicides can cause fungal pathogens like Candida tropicalis to change their genetic structure and become resistant to clinical antifungal drugs. When exposed to agricultural azole fungicides, these fungi can shift from their normal two-copy genetic state to a one-copy state, making them harder to treat with hospital medicines. This study reveals how the same drugs used on farms can create dangerous drug-resistant fungi that threaten human health.

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Exposure to Tebuconazole Drives Cross-Resistance to Clinical Triazoles in Aspergillus fumigatus

Farmers use a fungicide called tebuconazole to protect crops, but this chemical is similar to medicines doctors use to treat serious fungal infections in patients. A new study shows that when the fungus Aspergillus fumigatus is exposed to tebuconazole, it becomes resistant not just to this pesticide, but also to the clinical antifungal drugs used in hospitals. The fungus develops resistance mechanisms that allow it to survive high doses of these medications. This research highlights an important public health concern: the overuse of similar chemicals in agriculture can undermine our ability to treat dangerous fungal infections in people.

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Computational analysis of missense mutations in squalene epoxidase associated with terbinafine resistance in clinically reported dermatophytes

Certain fungal skin infections are becoming resistant to terbinafine, a common antifungal medication, due to genetic mutations in an enzyme called squalene epoxidase. Using computer models and analysis tools, researchers identified which mutations most strongly reduce the drug’s effectiveness and where the protein changes occur. Four specific mutations were found to prevent terbinafine from binding to its target, offering insights that could help develop better antifungal treatments.

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