Yersinia pestis—the bacterium that causes the bubonic plague—experienced a genetic tweak that allowed rodents to live longer after they were infected, according to a new study. This alteration may have prolonged two significant plague pandemics, including the deadliest event in human history: the Black Death.
Researchers at the Institut Pasteur in France and McMaster University in Canada studied hundreds of ancient Y. pestis DNA samples to investigate a gene called “pla.” Their study, published May 29 in the journal Science, identified a decrease in repetitions of the pla gene in the Y. pestis genome during the later stages of both the first and second major plague pandemics. The researchers believe these pla depletions ultimately allowed these pandemics to last longer.
The first plague pandemic, known as the Plague of Justinian, struck the Mediterranean basin during the sixth century and caused tens of millions of deaths over the course of two centuries. The second emerged when the Black Death broke out in 1347, killing an estimated 30% to 50% of Europe’s population in just six years. But this was just the beginning. Like the first pandemic, this plague continued to reemerge for centuries, lasting more than 500 years.
This newly discovered evolution of the pla gene offers more insight into how these plagues persisted for so long. The pla gene appears many times in the Y. pestis’ genome and plays a crucial role in its virulence by allowing it to infect the lymph nodes before traveling to the rest of the body, according to an Institut Pasteur statement. This causes rapid septicemia—or blood poisoning—and quickly kills the victim. Therefore, a lack of this gene in Y. pestis strains from the first and second major pandemics likely made the bacterium less virulent, the researchers suggest.
To test that hypothesis, they infected mice with three preserved strains of Y. pestis from the third major pandemic that also had fewer repetitions of pla. “These three samples enabled us to analyze the biological impact of these pla gene deletions,” said co-author Javier Pizarro-Cerdá, director of the Yersinia Research Unit at the Institut Pasteur, according to the statement.
Through their mouse model, Pizarro-Cerdá and his colleagues found that the pla depletion resulted in a 20% decrease in victim mortality. What’s more, it allowed infected rodents to live significantly longer. Based on these findings, the researchers concluded that rats infected with pla-depleted Y. pestis strains may have been more effective disease vectors, as they had more time to spread the plague far and wide before they died.
Rodents—particularly rats—played a critical role in spreading the bubonic plague to humans. People most commonly contract this disease via infected flea bites, and fleas typically contract it when they feed on infected rodents. Thus, an increase in the lifespans of sickened rodents would have provided greater opportunity for fleas to bite them, become infected, and then bite humans.
“Ours is one of the first research studies to directly examine changes in an ancient pathogen, one we still see today, in an attempt to understand what drives the virulence, persistence, and eventual extinction of pandemics,” said co-lead author Hendrik Poinar, director of the McMaster Ancient DNA Centre and holder of the Michael G. DeGroote Chair in Genetic Anthropology, according to the statement.
Today, the bubonic plague is considered a rare disease, though a small number of cases still emerge in western North America, Africa, Asia, and South America, according to the Cleveland Clinic. While this research provides valuable insight into the evolutionary history of Y. pestis and the world-altering pandemics it caused, it can also serve as a model for better understanding how deadly diseases emerge and spread, according to the researchers.
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