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Solved: The mystery of flesh-eating bacteria's relentless attack

tococcus that could not produce ScpC. As expected, this strain was much less virulent than the original M14. Only three of 28 mice receiving the mutant strain succumbed to infection, a death rate much lower than that of mice who received the original strain. Mice receiving the original bacteria developed lesions that grew until the mice died; while mice receiving the mutant strain developed only small lesions that spontaneously healed.

"The experiments show that SilCR downregulates the production of ScpC, and ScpC is what destroys the interleukin-8," said Hanski. "In our strain, M14, SilCR is missing completely, which explains why it is so virulent."

He said the work points to more effective strategies for treating Streptococcus infection. "There are different avenues you could explore for treatment, all based on reducing the amount of ScpC the bacteria produces," Hanski said. "You could look for a specific inhibitor of ScpC, or you could explore the activity of SilCR more fully and try to boost its action."
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Source:Howard Hughes Medical Institute


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