Genetic Changes in Bubonic Plague Bacterium Linked to Prolonged Pandemics
Yersinia pestis, the bacteria responsible for bubonic plague, underwent a genetic change that allowed infected rodents to survive longer, a new study suggests. This alteration might have contributed to two major plague pandemics, including the infamous Black Death.
Researchers from the Institut Pasteur in France and McMaster University in Canada explored hundreds of ancient Y. pestis DNA samples, focusing on a gene called “pla.” Their study, published on May 29 in the journal Science, revealed a reduction in repetitions of the pla gene in the Y. pestis genome during the later phases of the first and second significant plague pandemics. The researchers hypothesize that these changes ultimately contributed to the extended duration of these outbreaks.
The first pandemic, known as the Plague of Justinian, emerged in the Mediterranean during the sixth century, resulting in tens of millions of fatalities over two centuries. The second wave began with the Black Death in 1347, which wiped out about 30% to 50% of Europe’s population within six years. Notably, like the first, this plague kept reoccurring for centuries, stretching beyond 500 years.
This newly identified evolution of the pla gene sheds light on the persistence of these plagues. The pla gene is prevalent in the Y. pestis genome and is vital for its virulence, enabling the bacteria to infect lymph nodes before spreading throughout the body, as noted in a statement by the Institut Pasteur. This rapid action leads to septicemia, resulting in quick fatalities. So, a diminished amount of this gene in strains from the earlier pandemics likely reduced the bacteria’s virulence, the researchers suggest.
To explore this idea further, they infected mice with three preserved strains of Y. pestis from the third pandemic that also exhibited fewer repetitions of the pla gene. “These samples helped us evaluate the biological implications of these deletions in the pla gene,” said co-author Javier Pizarro-Cerdá from the Institut Pasteur.
Through their studies on the mice, the team found that the reduction in pla resulted in a 20% drop in mortality rates. Furthermore, infected rodents lived significantly longer, which led the researchers to conclude that rats infected with pla-depleted Y. pestis strains might have acted as more efficient disease carriers, given they had more time to spread the plague before dying.
Rats played a crucial role in transmitting the bubonic plague to humans. The disease is primarily contracted through infected flea bites, with fleas typically getting infected by feeding on diseased rodents. Therefore, an increase in the lifespan of infected rodents would provide more chances for fleas to bite them, get infected, and subsequently bite humans.
“This research is among the first to directly investigate changes in an ancient pathogen, with a goal of understanding what drives virulence, longevity, and eventual decline of pandemics,” said co-lead author Hendrik Poinar, director of the McMaster Ancient DNA Centre, in a statement.
Currently, bubonic plague is deemed rare, although a few cases continue to arise in western North America, Africa, Asia, and South America, according to the Cleveland Clinic. While this research offers valuable insights into the evolutionary path of Y. pestis and the massive pandemics it led to, it can also serve as a framework for gaining a better understanding of how severe diseases emerge and spread.
