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Disabling key protein may give physicians time to treat pneumonic plague

St. Louis, Jan. 23, 2007 -- The deadly attack of the bacterium that causes pneumonic plague is significantly slowed when it can't make use of a key protein, scientists at Washington University School of Medicine in St. Louis report in this week's issue of Science.

Speed is a primary concern in pneumonic plague, which kills in three to four days and potentially could be used in a terrorist attack. The bacterium that causes plague, Yersinia pestis, is vulnerable to antibiotics, but by the time an unusual infection becomes evident, Yersinia often has gained an unbeatable upper hand.

"By the time most doctors recognize an infection as plague, rather than the flu, it's already too late to begin antibiotic treatment," says senior author William Goldman, Ph.D., professor of molecular microbiology. "That makes pneumonic plague a concern both because of its rare natural outbreaks, one of which began in the Congo in 2005, and because of its potential use as a bioweapon."

Yersinia is best known for causing the Black Death in the Middle Ages in Europe, when historians estimate it killed a third or more of the population. Depending on how Yersinia is introduced, the versatile pathogen can modify itself to infect the lungs (pneumonic plague), the lymph glands (bubonic plague), or the bloodstream and organs (septicemic plague). Bubonic plague was spread by bites from infected fleas; pneumonic plague can spread through droplets of moisture expelled by coughing and sneezing.

With pilot project funding from the Midwest Regional Center for Excellence in Biodefense and Emerging Infectious Diseases Research, Wyndham Lathem, Ph.D., a postdoctoral fellow in Goldman's laboratory, developed a mouse model of pneumonic plague and showed that it had many similarities to human infection. In mice, pneumonic plague causes the lungs to fill up with a fluid composed of bacteria, inflammatory cells and other substances. Shortly before infected mice die, the bacteria also b
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Contact: Michael C. Purdy
purdym@wustl.edu
314-286-0122
Washington University School of Medicine
25-Jan-2007


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