Dangerous microbes can evolve rapidly. When we throw antibiotics at them, new strains can quickly shrug off the drugs and cause untreatable cases of tuberculosis, gonorrhoea, or staph. But most microbes don’t cause disease. Many share our bodies and those of other animals, and these residents—our so-called microbiome—are important parts of our lives.
And they can evolve too.
A microbe can even evolve quickly from a parasite into an ally. Kayla King from the University of Oxford found an excellent example of this in the guts of nematode worms. She showed that a bacterium called Enterococcus faecalis, which causes mild disease, can suddenly turn into a protector if its host is challenged by another more dangerous threat, Staphylococcus aureus or Staph.
King began by infecting worms with either Enterococcus or Staph. The two microbes behaved very differently. Enterococcus caused mild infections, killing fewer than one in a hundred worms, and only then after a week. By contrast, Staph killed half the worms within a day and all of the after a second. When mixed, Enterococcus protected the worms from its more virulent peer, slashing the death rate from 52 percent to just 18 percent.
To see if this dynamic would change over time, King picked out some infected worms, removed Enterococcus from their bodies, grew the microbes up, and then fed them to another generation of worms. She repeated 15 times. And in each new round she added the Enterococcus to genetically identical worms from the same stock, along with the same strains of Staph.
By the experiment’s end, Enterococcus had become an exceptional guardian, saving all but one percent of its hosts. It had evolved the ability to produce large amounts of superoxides—highly reactive oxygen molecules that are toxic to many microbes, Staph included. Enterococcus, by poisoning its rivals, was saving the worms.
This change depended entirely on the presence of Staph. When King exposed 15 generations of worms to Enterococcus alone, the mildly harmful bacterium became slightly more harmful. “On its own, it’s a little bit of a parasite,” says King. “But when it interacts with this much more virulent organism, it shifts along the continuum to be much more beneficial.”
She was surprised at how quickly the protective powers evolved (within just five of the 15 generations), how total they were (almost all the worms survived), and how broad it was. She challenged the worms with seven different strains of Staph, including the drug-resistant MRSA strains that give us humans so much grief. The protective Enterococcus strains beat them all.
There are many examples of microbes protecting animal hosts from parasites and diseases by producing antibiotics. They can also protect us simply by taking up space or using up resources, leaving no opportunities for more dangerous microbes to invade, and no room for them to grow. “We often consider ways in which the microbiome directly impacts host responses to infections,” says Nichole Broderick from the University of Connecticut. “This paper [shows] how the community can evolve traits that indirectly benefit the host.”
Note: indirectly. Enterococcus wasn’t evolving to protect the worms. It was suppressing a competing microbe, and benefiting its host almost by accident. This isn’t a story of altruism or good will, but of incidental beneficence. (It’s the mirror of another effect that I’ve written about, where microbes become coincidentally better at harming us when they’re exposed to predators or stressful environments.)
King’s study illustrates two other crucial themes in the world of microbiomes. First, as I’ve stressed before, it’s extremely contextual. The same bacterium can be a harmful pathogen (a microbe that causes disease) in one context but a helpful mutualist when its host is challenged by an even worse enemy. Likewise, the insect bacterium Hamiltonella protects aphids from parasitic wasps and becomes commonplace when such wasps are abundant; but it exacts a cost upon its hosts and is lost when wasps are absent. There are no good bacteria or bad bacteria; they live their own lives, and their impact upon our lives depends on all kinds of circumstances.
Second, microbes evolve quickly. In doing so, they can change the lives of their hosts with equal speed. The worms in King’s experiment didn’t need to evolve their own defences against Staph infections when they had Enterococcus to take up the slack. This all happened in the confines of a laboratory, but you can easily imagine how wild worms that consumed the right strains of bacteria would suddenly become immune to some infections (just like some bugs can become instantly resistant to insecticides by swallowing the right microbes).
“We’ve taken a very reductive approach,” says King. “In the future, we want to understand how these interactions play out in a much more diverse community.” Such as those in our bodies, for example. What happens when thousands of species of native microbes are challenged by Staph and other pathogens? How would they evolve in response?
And could we, perhaps, develop ways of directing that evolution to improve our health? “It’s very speculative, but I’d hope this would get people thinking about the possibility of engineering microbes using their natural evolutionary potential,” says King.
For more about the defensive power of microbes, and their ability to quickly change the lives of their hosts, check out my book I Contain Multitudes, out on August 9.