MADISON Acinetobacter baumanni, a pathogenic bacterium that is a poster child of deadly hospital acquired infections, is one tough customer.
It resists most antibiotics, is seemingly immune to disinfectants, and can survive desiccation with ease. Indeed, the prevalence with which it infects soldiers wounded in Iraq earned it the nickname "Iraqibacter."
In the United States, it is the bane of hospitals, opportunistically infecting patients through open wounds, catheters and breathing tubes. Some estimates suggest it kills tens of thousands of people annually.
But like many species of bacteria, A. baumanni is a social creature. In order to unleash its pathogenic potential, current research suggests that it must accumulate into large colonies or aggregate into "biofilms." To do this, it uses a microbial trick called quorum sensing, where chemical signals are used by the bacterium to gather and sense a critical mass of cells, which then act in unison to exert virulence, which in human patients can manifest itself in the form of pneumonia as well as urinary tract and blood infections.
Interfering with the quorum sensing behavior, some scientists think, may prove to be the Achilles heel of A. baumanni and other microbial pathogens, and new research by chemists at the University of Wisconsin-Madison now gives traction to that idea.
In a study by UW-Madison chemistry Professor Helen Blackwell and her colleagues, and published online in the journal ACS Chemical Biology, certain small molecule chemicals that can disrupt quorum sensing in A. baumanni have been identified, providing a glimmer of hope that the stubborn pathogen can be tamed.
"Right now, there are no approved drugs out there to modulate (quorum sensing), explains Blackwell, a leading expert on the phenomenon in microbes. "The strategy is not to kill the bacterium, but to keep it from behaving badly."
|Contact: Helen Blackwell|
University of Wisconsin-Madison