Antibiotics save lives -- but using them also helps antibiotic-resistant strains evolve and spread. Each year, antibiotic-resistant bacteria infect some 2.8 million people in the United States, killing more than 35,000, according to the Centers for Disease Control and Prevention.
Infections by multidrug-resistant -- or MDR -- bacteria, which are resistant to two or more antibiotics, are particularly difficult to treat.
Scientists at the University of Washington and the University of Idaho have discovered just how readily MDR bacteria can emerge.
In a paper published April 6 in Nature Ecology & Evolution , the researchers report that, for a bacterial pathogen already resistant to an antibiotic, prolonged exposure to that antibiotic not only boosted its ability to retain its resistance gene, but also made the pathogen more readily pick up and maintain resistance to a second antibiotic and become a MDR strain.
The team's experiments indicate that prolonged exposure to one type of antibiotic essentially "primed" the bacteria. This priming effect made it more likely that the bacteria would acquire resistance to additional antibiotics, even in the absence of further antibiotic exposure, and helped the strain hold on to those antibiotic-resistance traits for generations.
Exposure to antibiotics appears to select indirectly for more stable antibiotic resistance systems. A more stable system in a strain will increase the chances that it will acquire resistance to multiple antibiotics." Benjamin Kerr, Study Co-Senior Author and Professor of Biology, University of Washington
Their findings also show how antibiotic exposure affects the evolutionary dynamics within bacteria.
"This could help explain not only the rise of multidrug resistance in bacteria, but also how antibiotic resistance persists and spreads in the environment -- in health care settings, in soil from agricultural runoff -- even long after the antibiotic exposure has ended," said co-senior author Eva Top, a professor of biology at the University of Idaho.
The researchers tested a common mechanism for the spread of antibiotic resistance: plasmids. These are circular strands of DNA that can contain many types of genes, including genes for antibiotic resistance. Bacteria easily share plasmids, even across species.
Yet plasmids have their downsides, and past research has shown that bacteria readily shed them.
"Even though they can carry beneficial genes, plasmids can also interfere with many types of processes inside a bacterial cell, such as metabolism or DNA replication," said lead author Hannah Jordt, a UW research scientist in biology. "So, scientists have generally thought of plasmids as costly and burdensome to the host cell."
The UW-University of Idaho team worked with E. coli cells containing a tetracycline-resistance plasmid and Klebsiella pneumoniae cells containing a chloramphenicol-resistance plasmid. Both hosts, which had not been grown in the presence of antibiotics before, showed no great loyalty to their plasmids.
After nine days in an antibiotic-free environment, the fraction of Klebsiella still harboring a plasmid dropped to less than 50%. For E. coli , less than 20% kept their plasmid. Related Stories
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