John Younger, M.D., M.S., an associate professor of emergency medicine at the U-M Medical School, leads the team, which includes members with training in medicine, mathematics, and chemical engineering. He says the team's model reveals that a bacterial bloodstream infection can be thought of a high-speed police chase in heavy traffic.
"The bacteria are each a micron across - a thousandth of a millimeter - and they're traveling at the same fast speeds - up to three feet per second - as other cells in the bloodstream, like red and white blood cells and platelets," he explains. "The white blood cells, which are the police of the body, are stuck in the same flow and can't 'change lanes' in the fast-moving traffic to capture and kill them."
That means the bacteria have to stick to the wall of a blood vessel before they can get caught, he says. And they're most likely to do that in the small blood vessels, or capillaries, within our organs or extremities.
Antibiotic drugs have been the standard treatment for these conditions since the drugs were developed in the mid-20th century. But because common bacteria have evolved to evade those drugs, antibiotics are becoming less and less effective against bloodstream infections.
Better treatment for bacteremia and sepsis, then, might include strategies that can help the body filter bacteria out of the bloodstream and into these areas.
In the paper published in Shock, Younger and his team describe their new model of bacterial infection of the blood and organs, which they validated through experiments in mice.
The model combines the physiology of a blood vessel, the fluid dynamics
of blood, and math-based models of how bacteria multiply and move between
the bloodstream and organs. It also allows the researchers to better
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