Research Keyword: Drug resistance mechanisms

Fungal Metabolomics: A Comprehensive Approach to Understanding Pathogenesis in Humans and Identifying Potential Therapeutics

This review explains how scientists use metabolomics—a technique that identifies all chemical compounds in organisms—to understand how fungi cause disease and resist medicines. Fungi produce many different chemicals that help them attack our bodies and survive treatments, but these same chemicals could also be used to create new medicines. By studying these fungal chemicals, researchers can develop better antifungal drugs and understand how fungi manage to evade our immune system.

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Aspergillus terreus sectorization: a morphological phenomenon shedding light on amphotericin B resistance mechanism

This study investigated why some strains of the fungus Aspergillus terreus are resistant to amphotericin B, an important antifungal medicine. Researchers compared a resistant strain with a mutated version that became susceptible to the drug. They found that certain genes called P-type ATPases are more active in resistant strains and may help the fungus pump ions and alter its cell membrane to survive the drug. Additionally, mutations in genes responsible for producing secondary metabolites were linked to the visible changes seen when fungal cultures degenerate.

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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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Drug repurposing to fight resistant fungal species: Recent developments as novel therapeutic strategies

Fungal infections are becoming increasingly difficult to treat due to growing drug resistance, affecting millions of people worldwide each year. This research collection explores creative solutions by repurposing existing medications and developing new combination therapies that work better together against resistant fungal species. Studies show promising results combining common antibiotics like minocycline with antifungal drugs, and natural compounds from traditional medicine show potential for treating hard-to-treat infections like Candida and Aspergillus.

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Evaluation of Antifungal Activity Against Candida albicans Isolates From HIV-Positive Patients with Oral Candidiasis in a Major Referral Hospital, West Java, Indonesia

This study examined fungal infections in HIV-positive patients suffering from oral candidiasis (mouth thrush) in Indonesia. Researchers identified the types of Candida fungi present and tested their resistance to four common antifungal medications. Most patients had Candida albicans, and while these fungi generally responded well to newer antifungal drugs like voriconazole and fluconazole, some showed resistance, particularly to fluconazole, suggesting the need for careful testing before prescribing treatment.

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

When farmers use antifungal pesticides called triazoles to protect crops, the fungi can develop resistance to these chemicals. This study found that when the fungus Aspergillus fumigatus is exposed to the agricultural triazole tebuconazole, it can become resistant not only to that pesticide but also to clinical triazole drugs used to treat human fungal infections. The resistant fungi maintain this resistance even when the pesticide is removed, suggesting that environmental pesticide use may threaten the effectiveness of medical antifungal treatments.

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Multi-omics Analysis of Experimentally Evolved Candida auris Isolates Reveals Modulation of Sterols, Sphingolipids, and Oxidative Stress in Acquired Amphotericin B Resistance

Researchers studied how the fungus Candida auris develops resistance to amphotericin B, an important antifungal drug. By evolving two laboratory strains of this fungus under drug pressure, they discovered two different ways the fungus can become resistant: one through stress management genes, the other through changes in its protective lipids. These findings help explain why some clinical infections with this dangerous fungus are so hard to treat.

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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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Healthcare-associated fungal infections and emerging pathogens during the COVID-19 pandemic

During the COVID-19 pandemic, fungal infections became a major health concern, especially in hospitalized patients. Treatments for COVID-19, such as steroids and immunosuppressive drugs, weakened patients’ immune systems, making them vulnerable to serious fungal infections like those caused by Candida auris. Current antifungal medications have significant side effects and many fungi are developing resistance, so scientists are urgently seeking safer and more effective antifungal treatments.

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Deletion of RAP1 affects iron homeostasis, azole resistance, and virulence in Candida albicans

Researchers found that a protein called Rap1 plays a critical role in how the dangerous fungus Candida albicans acquires and uses iron, which is essential for its survival in the human body. When the RAP1 gene was deleted, the fungus became much less virulent and lethal in infected mice, while paradoxically becoming more resistant to the antifungal drug fluconazole under iron-limited conditions. These findings suggest that targeting iron acquisition through Rap1 could be a new therapeutic strategy against serious fungal infections.

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