Researchers have shown that, outside of a few specific examples, antibiotics do not promote the spread of bacterial antibiotic resistance through genetic swapping, as previously assumed.

       While the overuse of antibiotics is undeniably at the heart of the growing global crisis, new research published online April 11, 2016 in Nature Microbiology suggests differential birth and death rates and not DNA donation are to blame. The results have implications for designing antibiotic protocols to avoid the spread of antibacterial resistance.

       According to Lingchong You, the Paul Ruffin Scarborough Associate Professor of Engineering at Duke University and lead author on the paper; bacteria, does not often share resistant genes with each other.

       Bacteria can swap DNA 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, researchers assumed that the drugs increased the amount of genetic swapping taking place. But Lingchong You thought maybe the drugs were killing off the two "parent" lineages and allowing a newly resistant strain to thrive instead.

       Allison Lopatkin, a doctoral student in You's laboratory and the lead author of the study said they have showed at the single-cell level that the exchange of resistant genes is not influenced by antibiotics at all, which is in contrast to the literature. Previous studies haven't been able to tease these two ideas apart and their work decoupled them.

       In their experiments, Bacterial cells were put under a sort of suspended animation where they could neither die nor reproduce but they could still swap genes. With the birth and death rates no longer a variable, the researchers could see how the rate of gene exchanges responded to antibiotics.

       They tested nine clinical pathogens commonly associated with the rapid spread of resistance and exposed them to ten common drugs representing each major class of antibiotics. The rates of gene exchange in each test remained flat and, in a few cases, actually decreased slightly as the concentration of antibiotics grew.

       Lingchong You points out that there are a few proven examples of antibiotics directly inducing the expression of the genes responsible for donating resistance, but they are very specific. For example, the antibiotic tetracycline induces the expression of genes that only transfer tetracycline resistance.

       The new study shows that despite these outliers, antibiotics don't promote resistance spread by inducing global changes at the cellular level. The researchers hope further research will soon help clinicians to design better antibacterial protocols.

Antibiotics can lead to increased populations of resistant bacteria through changes in death-rates rather than an increase in the swapping of resistant genes. (Image credit: Duke University)

Source: www.sciencedaily.com