A genetic mechanism that controls the production of a large spike-like protein on the surface of Staphylococcus aureus (staph) bacteria alters the ability of the bacteria to form clumps and to cause disease, according to a new University of Iowa study.
The new study is the first to link this genetic mechanism to the production of the giant surface protein and to clumping behavior in bacteria. It is also the first time that clumping behavior has been associated with endocarditis, a serious infection of heart valves that kills 20,000 Americans each year. The findings were published in the Dec. 2103 issue of the journal PLOS Pathogens.
Under normal conditions, staph bacteria interact with proteins in human blood to form aggregates, or clumps. This clumping behavior has been associated with pathogenesis -- the ability of bacteria to cause disease. However, the mechanisms that control clumping are not well understood.
In the process of investigating how staph bacteria regulate cell-to-cell interactions, researchers at the UI Carver College of Medicine discovered a mutant strain of staph that does not clump at all in the presence of blood proteins.
Further investigation revealed that the clumping defect is due to disruption of a genetic signaling mechanism used by bacteria to sense and respond to their environment. The study shows that when the mechanism is disrupted, the giant surface protein is overproduced -- giving the cells a spiny, or "porcupine-like" appearance -- and the bacteria lose their ability to form clumps.
Importantly, the researchers led by Alexander Horswill, PhD, associate professor of microbiology, found that this clumping defect also makes the bacteria less dangerous in an experimental model of the serious staph infection, endocarditis.
Specifically, the team showed that wild type bacteria cause much larger vegetations (aggregates of bacteria) on the heart valves and are mor
|Contact: Jennifer Brown|
University of Iowa Health Care