The entire family tree of the Black Death has been mapped by scientists to better understand how the bubonic plague evolved to become so deadly.
Researchers at the Wellcome Trust Sanger Institute in Cambridgeshire have for the first time looked at the whole family tree of Yersinia pestis, the bacterium responsible for the bubonic plague, and Yersinia enterocolitica, a major cause of gastroenteritis.
Published in the Proceedings of the National Academy of Sciences, the authors found the pathogenic family members do not share a recent common disease-causing ancestor. Rather, they discovered a parallel evolutionary path that made them become harmful.
Previous focus on the harmful strains of the family, including the Black Death, has resulted in a fragmented understanding of the bacteria's evolution.
First author Sandra Reuter explained: "In order to understand how an organism becomes dangerous or pathogenic, we need to understand their non-pathogenic family members to see what makes them different.
"Our dataset has allowed us to redefine the family structure of this unique set of bacteria and give us a full view of how an individual bacterial species can become harmful."
Findings showed both harmful species evolved independently of one another, both acquiring a segment of DNA called plasmids and a gene that allowed them to become pathogenic.
They found that as well as the acquisition of genes, the loss of genes caused their deadly nature by streamlining their metabolic pathways.
After examining 224 strains of different Yersinia family members from across the world, they found that many of the metabolic functions lost by the pathogenic species were ancestral.
Senior author Alan McNally said: "We commonly think bacteria must gain genes to allow them to become pathogens. However, we now know that the loss of genes and the streamlining of the pathogen's metabolic capabilities are key features in the evolution of these disease-causing bacteria. This study is shifting our view of the evolution and relationship between species within one family of bacteria."
Nicholas Thomson, who was also senior author on the paper, added: "Before this study, there was uncertainty about what path these species took to become pathogenic: had they split from a shared common pathogenic ancestor? Or had they evolved independently. What we found were signatures in their genomes which plot the evolutionary path they took.
"Surprisingly they emerged as human pathogens independently from a background of non-pathogenic close relatives. These genetic signatures mark foothold moments of the emergence of these infamous disease-causing bacteria."