Yersinia pestis, the bacteria that caused Justinian’s Plague and the Black Death, was once only able to cause a mild gastrointestinal infection. However, researchers have found that a single genetic change to bacteria turned into one of the deadliest diseases in human history.
The article ‘Early emergence of Yersinia pestis as a severe respiratory pathogen’ by Wyndham Lathem and other researchers at Northwestern University’s Feinberg School of Medicine in Chicago, has just been published in the journal Nature Communications. The team was able to examine various historical forms of Yersinia pestis, and noticed that most versions could enter the lungs but cause no problems there. The exception were those forms of the bacteria that had a gene called Pla, which deals with breaking down blood clots.
The researchers then tested the bacteria, with and without the Pla gene, on mice and found that those with the extra gene produced a fatal lung infection.
Lathem, an assistant professor in Microbiology-Immunology at Northwestern University, explained “Our findings demonstrate how Yersinia pestis had the ability to cause a severe respiratory disease very early in its evolution. This research helps us better understand how bacteria can adapt to new host environments to cause disease by acquiring small bits of DNA.”
The researchers believe that the genetic change to Yersinia pestis took place about a century before the first major outbreak of disease in Europe, Justinian’s Plague, which took place between 541 and 542 AD. “Our data suggests that the insertion and then subsequent mutation of Pla allowed for new, rapidly evolving strains of disease,” Lathem added.
The paper also warns that other bacteria could be changed in the future in ways which could lead to similar outbreaks. The researchers note that a “single gene acquisition events have been demonstrated to have fundamental effects on an organism’s evolutionary adaptation to new hosts. Indeed, our data suggest that the emergence of other new respiratory pathogens could occur similarly via relatively small gene acquisition events.”