Researchers at Saint Louis University recently discovered new information regarding how antibiotics stop staph infections (staphylococcus aureus) and why staph sometimes become drug-resistant.
Led by Mee-Ngan F. Yap, assistant professor of biochemistry and molecular biology at SLU, researchers found evidence that suggests a mechanism in the bacteria strain prevents antibiotics from working in staph infections.
These findings, recently published in the "Proceedings of the National Academy of Sciences," now offer scientists a way to improve antibiotics so they won't become resistant to staph infections.
Yap and colleagues studied staph that had been treated with azithromycin. They found out that the antibiotic isn't as effective as was previously thought and that the process the bacteria use to avoid the antibiotic appears to be an evolutionary mechanism that the bacteria developed in order to delay genetic duplication.
"Here we describe, to our knowledge, the first genome-wide snapshot of ribosome distribution along messenger RNAs in Staphylococcus aureus," Yap said. "By globally mapping the position of stalled ribosomes in azithromycin-treated staph, we identified the proteins affected by this antibiotic. Our results reveal a striking similarity of stalling motifs that strongly suggests a universal stalling mechanism."
As the bacteria's ribosome replicates the strands of genetic code, ribosome stalling at upstream elements can promote the rearrangement of messenger RNA and can activate downstream translation of the resistance gene.
Further, it was discovered that the azithromycin-bound ribosomes do not stall at random residues, but only at specific sites. These residues have also shown to be the site in the ribosome stalling situations that inhibit genetic activity.