Candida albicans is widespread among humans, but normally does not affect health other than as vaginal or oral yeast infections, also called thrush.
But in medical settings, C. albans is a peril for sick people or individuals whose immune system has been compromised by cancer, HIV or organ transplant.
It accounts for one in every four hospital-acquired infections, often through plastic surfaces implanted in the body such as catheters, prosthetic joints or heart devices.
In the severest cases, nearly half of those infected die.
Adding to the problem is that C. albicans is a stealthy foe, able to change the structure of its cell wall to outsmart new drugs.
The latest research, published in a US journal on Monday, highlights a promising target: the mechanism that the yeast uses to latch on to human cells and colonise them, thanks to a tiny part of a protein call Als adhesin.
"Als adhesin proteins give the yeast an ability to thrive throughout the human body, which is what makes it such a dangerous infections," said Ernesto Cota, a medical biologist at Imperial College London.
Cota`s team used hi-tech scanners to probe the structure of the elusive protein.
The next step is to test experimental compounds on lab-dish samples of the fungus to see whether this will block the binding action.
The study appears in Proceedings of the National Academy of Sciences (PNAS).