It sure looks that way. Last night, I was talking to a colleague and he told me that several groups, including his, are seeing a very interesting pattern in commensal Escherichia coli (those E. coli that live in everyone’s gut and aren’t making us sick).
In humans, it appears that roughly 20% of all commensal E. coli belong to one of three clones that have a global distribution (in bacteriology, a clone is a group of very closely related strains). (an aside: In animals, there doesn’t appear to be this skewed pattern. In animals, the distribution of clones appears to be more evenly distributed, with no predominant clones.)
This is interesting because we see the same pattern of epidemic spread with pathogenic (disease-causing) bacteria in humans. With methicillin resistant Staphylococcus aureus (MRSA), there are often a few predominant clones (or even one) that is extremely common. The rise of vancomycin resistant enterococci (VRE) in Europe was largely due to the spread of one clonal type (frighteningly, it appears that an identical pattern of VRE spread is beginning to repeat itself in the U.S. And we do nothing).
So it looks like there’s something about human populations that predisposes human microbial fauna towards a pattern of epidemic spread, even when the bacterium isn’t causing any disease. Hopefully, as the cost of molecular epidemiology decreases, we’ll be able to determine whether this pattern holds up. Since so many species of bacteria that cause disease are often commensals, and not ‘strict’ pathogens (e.g., S. aureus, Enterococcus, Streptococcus pneumoniae, and E. coli), we really need to focus more of our efforts on understanding the biology of the commensal strains of ‘pathogenic’ bacteria, especially since the commensals are the majority in these species.