Context
Fungal infections are becoming an important public-health challenge as disease-causing fungi increasingly develop resistance to commonly used antifungal drugs. New research on Candida auris shows that fungi can escape medicines not only through genetic mutations but also by making additional copies of protective genes and even chromosomes. This suggests that simply developing stronger antifungal drugs may lead to a continuing evolutionary “arms race”.
Explanation
- Fungi are a diverse group of eukaryotic organisms, separate from plants and animals, and include yeasts, moulds and mushrooms. Candida auris is an emerging pathogenic yeast capable of causing serious hospital-acquired and multidrug-resistant infections.
- Multiple routes to drug resistance: Fungi can survive antifungal medicines through gene mutations, gene duplication and changes in chromosome number.
- More drug does not always mean better treatment: At unusually high concentrations of some antifungal drugs, fungi may activate compensatory survival mechanisms, such as increasing production of chitin in their cell wall. This paradoxical survival at high drug doses is sometimes called the Eagle effect.
- Climate change–health linkage: Rising temperatures may favour heat-tolerant fungi. Since many fungi normally cannot survive at human body temperature, global warming could potentially increase the number capable of infecting humans.
- Antifungal resistance is part of the wider AMR challenge. Hospitals therefore require susceptibility testing and genomic surveillance to determine which drugs will work against particular fungal strains.
- Instead of continuously escalating the chemical “arms race”, researchers suggest combination therapies and drugs targeting less evolutionarily critical pathways, so that fungi have less incentive or ability to develop resistance.
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