In the early, most explosive stages of the Black Death, the pla gene was found in high copy numbers. In this state, the disease was exceptionally virulent. It moved through the body with terrifying speed, killing its hosts quickly and with a high degree of certainty. However, the genetic analysis revealed a surprising shift: in later outbreaks of the same pandemic, the number of pla copies began to decrease.
This reduction in the gene’s presence had a profound effect on the disease’s behavior. In laboratory models using mice, the researchers observed that a lower pla copy number decreased mortality by approximately 20 percent. More importantly, it increased the duration of the infection. The hosts lived longer before succumbing to the disease, a change that, while seemingly beneficial to the host, was actually a calculated evolutionary move by the pathogen.
This discovery highlights a classic biological trade-off. A pathogen that kills its host too quickly risks "burning out" before it can be transmitted to a new victim. By reducing its virulence and allowing the host to survive longer, Y. pestis ensured it had a greater window of opportunity to spread.
The researchers noted a striking pattern: in both the Justinian Plague and the Black Death, this evolutionary reduction in pla copy numbers occurred approximately 100 years after the initial outbreaks. This suggests that the bacterium was reacting to its environment, finding a "sweet spot" of lethality that maximized its reproductive success. When the gene copy number dropped and the infected rats lived longer, they could travel further and interact with more of their kind, effectively ensuring the plague’s continued presence in the environment.
"The reduction of pla may reflect the changing size and density of rodent and human populations," says Poinar. "It’s important to remember that plague was an epidemic of rats, which were the drivers of epidemics and pandemics. Humans were accidental victims."
The role of the black rat (Rattus rattus) is central to this narrative. In the crowded cities of the medieval and early modern periods, these rats served as "amplification hosts." Because black rats are highly susceptible to Y. pestis, the pathogen required a stable and high-density rat population to thrive. If the plague killed the rats too fast, the fleas—the primary vectors that jump from rats to humans—would lose their hosts, and the cycle would break. By evolving to be slightly less lethal to the rats, the plague could maintain a steady reservoir of infection.
However, this evolutionary path eventually led to a dead end for certain strains. The study found that while one lineage of the second pandemic evolved into the ancestor of all modern-day strains, another lineage—the one that had undergone significant pla reduction in Europe—eventually went extinct by the early 19th century. This extinction likely reflected a final shift in the host-pathogen relationship, where the environment or the host populations changed so much that even the attenuated version of the bacteria could no longer survive.
