Aside from those of us with access to microscopes, most people will never see microbes with their own eyes. And so we tend to identify microbes with the disease-causing minority among them, the little buggers that trigger the tickling mist of a sneeze or the pustule on otherwise smooth skin. We become aware of their existence when they threaten our lives, and for much of our history, that threat was substantial. Epidemics of smallpox, cholera, tuberculosis, and plague have traumatised humanity, and the fear of these diseases has contaminated our entire culture, from our religious rites to Hollywood films such as Contagion (2012) or Outbreak (1995).
When microbes aren’t killing us, we are largely oblivious to them. So, we construct narratives of hosts and pathogens, heroes and villains, us and them. Those that cause disease exist to reproduce at our expense, and we need new ways of resisting them. And so we study how they evolve to outfox our immune system or to spread more easily from one person to another. We identify genes that allow them to cause disease and we label those genes as ‘virulence factors’. We place ourselves at the centre of their world. We make it all about us.
But a growing number of studies show that our anthropocentric view is sometimes unjustified. The adaptations that allow bacteria, fungi and other pathogens to cause us harm can easily evolve outside the context of human disease. They are part of a microbial narrative that affects us, and can even kill us, but that isn’t about us. This concept is known as the coincidental evolution hypothesis or, as the Emory University microbiologist Bruce Levin described it in 2008, the ‘shit happens’ hypothesis. [Continue reading…]