Rice University lab identifies mutations that allow bacteria
to resist antibiotics
(August 5, 2015) Rice
University scientists are developing strategies to keep germs from evolving
resistance to antibiotics by heading them off at the pass.
The Rice lab of biochemist Yousif Shamoo identified a
genetic mechanism that allows bacteria to develop resistance while
simultaneously and quickly spreading the capability to others in a population.
“This is really a double whammy,” Shamoo said. “Our finding
that these bacteria become more antibiotic-resistant while at the same time
spreading their resistance more efficiently was really surprising and
worrying.”
The researchers hope this knowledge will help predict when
and how bacterial strains are likely to develop resistance to future
antibiotics and perhaps act to halt — or at least slow — the process. The
research appeared in the journal Molecular Biology and Evolution.
Antibiotic resistance is responsible for hundreds of
thousands of infections acquired in American hospitals, according to the
Centers for Disease Control and Prevention. These infections kill thousands of
patients. While progress is being made to control microbes that spread
infection, the overriding concern remains that drugs developed to kill germs
will ultimately stop working.
Until now, the only effective way to keep antibiotics from
losing their potency has been to use them sparingly, said Kathryn Beabout, a
Rice graduate student and lead author of the new paper.
“The best you can do is try to manage when you use the
antibiotic,” she said. “But our idea is that if we can predict how resistance
is going to emerge, we can come up with strategies to use antibiotics in a more
intelligent way.”
The lab used experimental evolution to study a specific
combination of bacteria and an antibiotic that had not been in common contact.
The bacteria of interest was Enterococcus faecalis, found in the
gastrointestinal tract. The antibiotic was tigecycline, a highly effective but
sparingly used derivative of tetracycline. The goal was to see how horizontal
gene transfer – the means by which cells pass along favorable mutations – would
work in the presence of the antibiotic.