A well-accepted principle in the animal kingdom is that creatures already occupying a habitat nearly always prevail over competitors from the same species that arrive later. While the mechanisms that enable "owners" to outcompete "intruders" typically involve a brain that drives such behavior, a new study led by researchers at NYU School of Medicine found this principle to be in play in some bacteria as well—bacteria that declare "ownership" of human host tissue to rival strains.
Results of the study, published today in Nature Microbiology, argue that whatever strain of Streptococcus pneumoniae is in place in a mammal's tissues first is the one more likely to thrive than Strep "latecomers."
"With Strep infections costing the lives of nearly a million children under five each year globally, we are urgently seeking new ways to defeat bacteria by learning more about how they compete with each other," says senior study author Jeffrey Weiser, MD, chair of the department of microbiology at NYU Langone Health.
Past studies have established that bacteria engage certain mechanisms only when an infection matures to the point where the bugs have multiplied beyond a population density threshold, known as a "quorum." The new study suggests that among the mechanisms initiated by a Strep quorum is release of two toxins—choline binding protein D (CbpD) and the competence-induced bacteriocins (CibAB). These toxins kill intruding, competing strains. The owners, however, also release other factors that protect them from their own toxins. Their newly arriving relatives, not yet having a quorum, do not yet have their defenses in place.
Still other studies have pointed to the concept that once the intruder bacteria die, they burst and spill their DNA into the extracellular space. This enables the bacteria that killed them to "sample" their DNA, pulling in and using any genes that help the owner to survive, or to defeat antibiotics.
Related to this process is the idea of "competence," or the ability of a bacterial cell to incorporate foreign DNA, a function that is regulated in Strep by a set of genes called the competence regulon.
Pulling all of these factors together, the new study finds that the mechanism conferring advantage on owner strains is, in fact, the quorum-sensing, competence regulon-induced production and release of bacteriocins like CibAB to kill newly arriving competitors.
The team also used mathematical modeling to support the idea that competence regulon activation has a significant role in competition for dominance, even for strains with different competitive advantages, and that owner dominance manifests quickly.
Image: The image shows Strep bacteria strains (in red) competing to colonizing the airway surface in mice. Image courtesy of NYU Langone Health.