A bout of Salmonella food poisoning isn’t a pretty affair. Your digestive tract churns, you can’t keep your food down, and you feel exhausted. But you aren’t the only one affected. Your gut contains trillions of bacteria, which outnumber your own cells by ten to one. They are your partners in life, and they are also transformed by the presence of the invading Salmonella.
Minority members of this intestinal community start to bloom, greatly increasing in number as the guts around them become inflamed. And these gut bacteria start to trade genes with Salmonella.
These swaps are a regular part of bacterial life. In their version of sex, two cells become united by a physical bridge, through which they shunt rings of DNA called plasmids. These rings can act like mobile weapons packages. Some give otherwise harmless bacteria the ability to cause disease. Others confer resistance to antibiotics. It’s a network of shady arms trading, and in your inflamed bowels, it happens at an unprecedented level.
The microbes in our guts include species such as Escherichia coli, which normally behave as peaceful citizens but occasionally cause disease. These ‘enterobacteria’ make up just a tiny proportion of the entire community, and their numbers are suppressed by the more common bacteria in the guts. Their rarity effectively stops them from trading genes with one another, since they need to actually touch for that to happen. That’s good. It stops the Jekyll-like bacteria from picking up genes that could turn them into Hyde-like monsters, like the E.coli strain that killed 45 Germans last year.
This tranquil picture changes when infectious bacteria enter it. Barbel Stecher from ETH Zürich showed that when mice are infected with Salmonella, the native E.coli in their guts start to bloom as well. Once mere bit-players, their numbers go up by more than 100 times. In some cases, E.coli accounted for more than 80 percent of the bacteria in the rodents’ guts.
Stecher found that several of the E.coli strains in this melange carried a plasmid that’s 99% identical to one normally borne by Salmonella. Known as P2, it includes several genes that allow bacteria to resist antibiotics. The E.coli probably picked up this plasmid from the Salmonella which had suddenly joined them. After all, the mice in the study had been reared in faultlessly clean and carefully monitored conditions. It’s unlikely that they had been exposed to any Salmonella before the experiment.
Blecher infected sterile mice with a strain of Salmonella that had P2, and one of the earlier E.coli strains that did not. She waited. Both species of bacteria bloomed and within four days, virtually every single E.coli had picked up the P2 plasmid from its neighbours. Bacteria pass genes to each other all the time, but in these infected guts, it happened with an efficiency that’s practically unheard of.
Blecher’s study shows that the harmless bacteria in our bodies are intimately connected with the disease-causing ones that invade us from the outside. A bout of disease can influence the evolution of both groups. Infectious bacteria aren’t just making us ill – they’re also weaponizing our allies.
Reference: Stecher, Denzler, Maier, Bernet, Sanders, Pickard, Barthel, Westendorf, Krogfelt, Walker, Ackermann, Dobrindt, Thomson & Hardt. 2011. Gut inflammation can boost horizontal gene transfer between pathogenic and commensal Enterobacteriaceae. PNAS http://dx.doi.org/10.1073/pnas.1113246109
An introduction to the microbiome