The exponential rise of antibiotic drug resistance is a considerable threat to global public health. Researchers are continually searching for the underlying mechanisms that promote this resistant phenotype. Some evidence exists to suggest that antibiotic use encourages the spread of bacterial resistance through genetic swapping. However, new research suggests that these examples are outliers and not indicative of the majority of bacterial populations.
Researchers at Duke University suggest that differential birth and death rates of microbes and not DNA donation are to blame. The results have implications for designing antibiotic protocols to avoid the spread of antibacterial resistance.
"The entire field knows there's a huge problem of overusing antibiotics," noted senior study author Lingchong You, Ph.D., associate professor of engineering at Duke University. "It is incredibly tempting to assume that antibiotics are promoting the spread of resistance by increasing the rate at which bacteria share resistant genes with each other, but our research shows they often aren't."
Investigators have known for decades that bacteria can swap genetic elements through a process called conjugation, which allows helpful genes to spread quickly between individuals and even between species. Because the number of resistant bacteria rises when antibiotics fail to kill them, many researchers have assumed that the drugs increased the amount of genetic swapping taking place. The Duke researchers, however, hypothesized that the antibiotics were killing off the two "parent" lineages and allowing a newly resistant strain to thrive instead.
