A dangerous hospital fungus has evolved a cunning strategy to thrive on human skin, and scientists have unraveled its secret. This notorious pathogen has learned to feed on the carbon dioxide we exhale, giving it a metabolic edge that allows it to persist and spread unnoticed.
The fungus, known as Candida auris, has developed a unique ability to survive on the skin's surface, where it can easily spread from person to person without causing immediate illness. This silent colonization is a major concern, as it can lead to dangerous infections, especially in healthcare settings.
But here's where it gets controversial: Researchers have discovered that a single enzyme, carbonic anhydrase, is the key to this fungus's success. This enzyme allows Candida auris to convert the small amounts of CO2 present on the skin into usable fuel, keeping its mitochondria running even when other nutrients are scarce. This metabolic trick not only helps the fungus endure treatment but also explains why it can colonize the skin so effectively.
The team's findings suggest that targeting this CO2-powered pathway could be a game-changer in preventing infections. By blocking carbonic anhydrase, the fungus struggles to establish itself, offering a potential new strategy to stop colonization in its early stages.
And this is the part most people miss: The skin's microbiome, the diverse community of bacteria and fungi that live on our bodies, plays a crucial role in providing CO2 for Candida auris. Some bacteria produce an enzyme called urease, which breaks down urea in sweat into ammonia and CO2, essentially feeding the fungus. Targeting bacterial urease could reduce CO2 levels on the skin, but any approach must be careful not to disrupt the beneficial microbes.
Inside the fungus, energy production relies on a chain of proteins, including a mitochondrial complex called cytochrome bc1. This complex proved to be a weak point, and inhibiting it made Candida auris more vulnerable to antifungal drugs like amphotericin B. This combination therapy could potentially extend the life of older drugs, but more research is needed to ensure its safety.
The colonization process happens in stages, and early intervention is key. When the CO2 pathway is disrupted, the fungus struggles to establish itself on the skin's surface, where food is scarce. However, once it reaches deeper areas like hair follicles, higher CO2 levels can compensate for the missing enzyme. This split highlights the importance of focusing prevention efforts on the first few days of colonization, when it is still fragile.
The risk of outbreaks in hospitals is a serious concern. Candida auris can silently spread through healthcare facilities, riding on symptom-free skin and seeding rooms and equipment. For patients with weakened immune systems, invasive infections can be deadly, with some reports showing death rates as high as 70%.
Hospitals currently use isolation rooms, gloves, and careful cleaning to combat the fungus, but these measures can be time-consuming. The World Health Organization has recognized the threat and added it to its global priority list for dangerous fungal infections. The new CO2 targets identified in this study offer extra tools to reduce the spread, but they do not replace the basics of infection control.
Treatment options remain limited, and clinicians must tread carefully to avoid pushing the fungus toward even broader resistance. For bloodstream infections, doctors often start with echinocandins, drugs that weaken fungal cell walls, but resistant cases are becoming more common. Amphotericin B is a powerful option, but it can damage the kidneys and requires close monitoring. If CO2-driven energy helps the fungus tolerate amphotericin B, combining it with energy blockers could restore sensitivity, but more research is needed.
This study highlights the importance of targeting colonization itself, as it links skin survival and drug tolerance to a shared energy pathway. The next step is to test these inhibitors in patients and ensure they are safe and effective in blocking the fungus without harming human cells.
The findings were published in the journal Nature, offering a fascinating insight into the complex world of fungal infections and potential new strategies for prevention and treatment.
