Because biofilms resist antibiotics, the only treatment is surgery to remove the contaminated device and implant a new one. This adds up to thousands of surgeries and more than $1 billion in health care costs every year.
A team led by scientists at Ohio State University and Duke University Medical Center used atomic force microscopy and powerful computer simulations to determine how Staph bacteria bond to the devices in the process of forming these biofilms.
The findings offer clues about potential techniques that could be employed to prevent infections in patients who need these devices to stay alive.
"We're probing the initial step to that biofilm formation," said Steven Lower, scientist at Ohio State and lead author of the paper reporting the study's results.
"Can you shut that down somehow? If that bacterium never sticks, there's no biofilm. It's that simple. But it's not quite that simple in practice."
Using Staph cells collected from patients--some with cardiac device-related infections--the researchers examined how these bacteria adhere to implants to create a biofilm.
The bond forms when a protein on the bacterial cell surface connects with a common human blood protein coating an implanted device.
But an estimated half of all Americans have Staph bacteria living in their noses, and not every cardiac implant patient develops an infection.
So why do some strains of these bacteria cause infection while others remain dormant?
The researchers discovered that Staph surface proteins containing three genetic variants, or single-nucleotide polymorphisms, formed stronger bonds with the human proteins than did Staph proteins without those variants.
The presence of these genetic variants was associated with the strains of bacteria that had infected implanted cardiac devices.
|Contact: Cheryl Dybas|
National Science Foundation