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Researchers find how some antibiotics kill bacteria

polymerase's molecular 'hood' we couldn't see what the problem was," she said. "We never suspected that removing this ion was what killed rifamycin-sensitive bacteria. But the resolution of previous atomic structures wasn't sufficient enough to see that."

The higher-resolution images also showed that rifapentin and rifabutin each bind just a little differently to E. coli, but still bring about the same results.

The answer to creating a new breed of bacteria-resistant antibiotics may lie in these variations in binding.

"From these findings we can suggest how rifamycins that are currently used in therapy can be improved to be effective even against existing resistant strains of bacteria," Artsimovitch said

Rifamycins are what drug companies call "broad-spectrum antibiotics." Not only are they effective against tuberculosis, they also act against a variety of other pathogens including Neisseria meningitidis, the bacterium that causes one form of meningitis; Helicobacter pylori, which causes stomach ulcers; and even some parasitic worms by eliminating the symbiotic bacteria parasites depend on.

"It's the kind of drug the pharmaceutical business wants to produce," Artsimovitch said. "They're looking for the broadest range of antibiotics possible. Rifamycins would be ideal drugs if we could figure out how to get rid of resistance."


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Source:Ohio State University


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