Inside our bodies, two dangerous pathogens have figured out how to do business with each other — and the currency they trade in is copper. Scientists at the University of Exeter have uncovered a surprising economic arrangement between the fungus Candida albicans and the bacterium Staphylococcus aureus, showing that these normally separate microbes cooperate by carefully managing copper levels in their shared environment. The discovery, published in the journal Microbiology, could point toward entirely new ways of dismantling stubborn infections that current treatments struggle to clear.
Both C. albicans and S. aureus are familiar troublemakers in hospitals and wounds. C. albicans causes yeast infections and can become systemic; S. aureus ranges from skin boils to life-threatening bloodstream infections. When they colonize medical devices or chronic wounds together, they form mixed biofilms — slimy, surface-attached communities that shrug off antibiotics in ways single-species infections cannot. The Exeter team, led by Dr. Seána Duggan from the MRC Center for Medical Mycology, wanted to understand why.
What they found was a kind of microbial diplomacy around a single element. When grown together in lab conditions designed to mimic the human body, the two species built larger, more active biofilms than either could manage alone. Protein analyses revealed why: C. albicans ramped up proteins dedicated to pulling copper in, while S. aureus cranked up proteins for exporting copper and protecting itself from copper stress. The fungus hoards the metal; the bacterium pumps it back out. Together, they maintain a careful equilibrium — a "copper economy" the researchers call it.
But this partnership has a fragility. When the researchers disrupted copper levels — adding too much or starving the system — the mixed biofilm fell apart. Neither excess nor scarcity spared the community. Critically, the combined biofilm was far more vulnerable to copper disruption than either organism growing solo.
"The most striking thing was that the mixed biofilm was much more sensitive to copper disruption than either organism alone," Duggan said. "That tells us we are not just looking at the biology of one pathogen or the other. We are looking at the biology of the relationship between them."
That sensitivity is the hopeful part. If copper imbalance can unravel these resilient partnerships, targeted copper-based therapies might eventually offer a way to break apart infections that now resist treatment. Duggan emphasized that the work argues for looking beyond single-pathogen models. Understanding what keeps microbes cooperating — and what makes them fail — could reshape how we fight complex infections.