Plasmids are mobile bits of DNA that play a key role in bacterial evolution. They shuttle genes for things like antibiotic resistance and pathogen virulence among different strains or species of bacteria. But not all plasmids carry these genes, and it’s been an outstanding question how plasmids persist in bacterial populations. One possibility is that they’re a kind of genetic parasite, slightly reducing the fitness of the cells they infect but continually infecting new bacteria. One problem with this idea, though, is that their infection rates often don’t seem high enough for a purely parasitic lifestyle.
A new paper by Bärbel Stecher and colleagues at ETH Zürich shows that when Salmonella infect mammalian guts they create an environment that drastically increases plasmid transfer among the bacteria there. They inflame the gut tissue, causing a “bloom” of resident E. coli. All those bacteria bump into each other more, allowing plasmids—which spread by direct contact between bacterial cells—to go gangbusters. The paper has a lot of good experiments showing that it’s the increased bacterial density, and not the inflammation, that causes increased plasmid transfer.
The implication is that plasmids can make a living as parasites if Salmonella and other pathogens cause enough gastrointestinal disturbance, as they might in the developing world or in nonhuman mammal populations. I did find overblown the authors’ claims that their findings “shift the current paradigm” because they show that Salmonella and E. coli share plasmids (which we already knew) and “boost” pathogen evolution (which their findings do not show), but overall this is a pretty cool paper.
Stecher B, Denzler R, Maier L, Bernet F, Sanders MJ, Pickard DJ, Barthel M, Westendorf AM, Krogfelt KA, Walker AW, Ackermann M, Dobrindt U, Thomson NR & Hardt W-D (2012) Gut inflammation can boost horizontal gene transfer between pathogenic and commensal Enterobacteriaceae. PNAS 109: 1269-1274.