Scientist finds way to improve antibiotics to treat staph infections

Assistant professor of biochemistry and molecular biology at Saint Louis University Mee-Ngan F. Yap, Ph.D studied staph that had been treated with the antibiotic azithromycin.

During the study she found that antibiotic isn’t as effective against staph and the process that the bacteria use to evade the antibiotic appears to be an evolutionary mechanism that the bacteria developed in order to delay genetic replication when beneficial.

Mee-Ngan F. Yap team carried out a study how antibiotics work within the ribosome, the site where bacteria translates the genetic codes into protein.

The study found that when the bacteria encounter a potential problem in copying its genetic material, as posed by an antibiotic, it has a mechanism to thwart antibiotic inhibition by means of "ribosome stalling" that is mediated by special upstream peptide elements, the scientists said.

The also found that many resistant pathogens exploit this mechanism to up-regulate antibiotic resistance genes and make them survive in the presence of antibiotics.

Delay in the effect of antibiotics also allows the bacteria to develop a defense against the antibiotic further down the line of genetic code.

Yap said, "Here we describe, to our knowledge, the first genome-wide snapshot of ribosome distribution along messenger RNAs in Staphylococcus aureus.

"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," Yap said. "We have identified what appears to be an evolutionary mechanism developed by bacteria to counteract the type of antibiotics that includes azithromycin, called macrolides."

Findings from the study have been published in Proceedings of the National Academy of Sciences.