More than 30 million Americans rely on implanted medical devices like prosthetic joints, pacemakers and more to improve their quality of life. But implanting any foreign object into the body also carries risk of introducing deadly fungal infections.
New research from University of Georgia scientists uncovers how a transcription regulator protein for the fungal pathogen Candida albicans coordinates a diverse set of genes to infect medical devices in the human body.
Candida albicans is typically a harmless yeast commonly found in the human body. But overgrowth of the fungus can lead to yeast infections, thrush or even potentially life-threatening invasive candidiasis that can lead to organ failure.
The medical devices that can potentially harbor infections include catheters, pacemakers, artificial heart valves and prosthetic joints.
“Overall infection rates vary … but hover around 500,000 to 1 million per year in the U.S.,” said Aaron Mitchell, senior author of the study and Distinguished Research Professor in the UGA Franklin College of Arts and Sciences department of microbiology.
Biofilms on medical devices pose infection risk
Medical devices provide an appealing surface for microorganisms to latch onto, and once these biofilms form, they’re hard to break through.
Biofilms release cells that infect deep tissue and are often unresponsive to antifungal therapy.
In the case of Candida albicans, biofilm formation requires coordination of gene sets for adherence, for cell development and maturation, and for growth in low-oxygen conditions. The new study shows that protein complexes of the transcription factor Ume6 coordinate expression of these gene sets.
The new findings focus on the protein Ume6, which may be considered a hitchhiker that interacts with other proteins to reach its destination.
Think of microbial biofilms … like kitchen wrap that allows a community of cells to stick together and often adhere to a surface.”
—Aaron Mitchell, Franklin College of Arts and Sciences
“Think of microbial biofilms less like a movie and more like kitchen wrap that allows a community of cells to stick together and often adhere to a surface if one is present, as in the case of an implanted device,” Mitchell said.
“Our findings here explain why Ume6 is so effective in driving biofilm and hypha formation: Its direct targets include numerous genes known to be required for these processes.”
Published in Nature Microbiology, the study was co-authored by UGA’s Eunsoo Do and Katharina Goerlich; Carnegie Mellon’s Joel McManus; Manning Y. Huang, formerly of Carnegie Mellon and now of University of California San Francisco; and the University of Wisconsin, Madison’s Robert Zarnowski and David R. Andes.
