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Staph’s Trail Points to Human Susceptibilities

Scientists have finally found an answer to one of the great mysteries about the most deadly bacteria, Staphylococcus aureus — why it attacks primarily humans and not animals. And they now have an idea of why some humans are particularly susceptible to these bacteria that kill 100,000 Americans a year, far more than any other microbe.

In a study released on Wednesday, researchers at Vanderbilt University report that staph evolved to zero in on particular regions of human hemoglobin so it could burst the cagelike molecule and feed on the iron inside. People who are resistant to staph, they suspect, might have slight genetic variations that tweak the hemoglobin regions the bacteria seek, making them impervious to the attack.

The work is part of a more general look at genes and disease. With new tools to look in detail at slight genetic variations, researchers are asking why some people get some diseases and others do not and why some die from diseases that others almost shrug off. With staph, for instance, 30 percent of the population harbors the bacteria in their noses, with no signs of infection.

Staph experts say the discovery, published in the Dec. 16 issue of Cell Host & Microbe, answers a lot of questions about the bacteria and shows them new directions for research.

“It’s terrific work,” said Frank DeLeo, acting chief of human bacterial pathogenesis at the National Institute of Allergy and Infectious Diseases. “It really is moving the field forward.”

The work began in 2002 when Eric P. Skaar was a postdoctoral fellow and fascinated by staph.

“Staph is the worst infectious threat to public health,” he said. “It is the No. 1 cause of heart infections and skin infections, the No. 1 cause of soft tissue infections. It is a big cause of pneumonia. It is the No. 1 hospital acquired infection.”
 
 

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