Researchers have plotted the entire family tree of the Black Death bacterium, to understand how some family members evolved to become so harmful.

Contrary to popular belief, it turns out that pathogenic members of this bacterial family do not share a recent common disease-causing ancestor, but oddly, have followed parallel evolutionary paths to become dangerous.

The Yersinia family of bacteria has many sub-species, some of which are harmful and others not.

Two of the most feared members of this bacterial family are Yersinia pestis, the bacterium responsible for the bubonic plague or the Black Death, and Yersinia enterocolitica, a major cause of gastroenteritis.

“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 to the pathogenic forms,” says Dr Sandra Reuter, first author of a new report on the topic.

“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.”

A team from a leading genome research centre sequenced 224 strains of different Yersinia family members from around the world to fully understand how specific species evolve.

The unique and detailed dataset they produced describes the parallel evolution of Yersinia pestis and Yersinia enterocolitica, showing that both species, independent of each other, acquired a segment of DNA known as plasmids, as well as the gene that allowed them to become pathogenic.

It appears that only these two virulence factors are present in all of the pathogenic Yersinia species.

“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” says Professor Nicholas Thomson, senior author of the report.

“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.”

By examining the genomes of both the pathogenic and non-pathogenic species, the team was able to determine that many of the metabolic functions, lost by the pathogenic species, were in fact ancestral.

These functions were probably important for growth in a range of niches, and have been lost rather than gained in specific family lines in the Yersinia family.

“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,” says Dr Alan McNally, senior author from Nottingham Trent University.

“This study is shifting our view of the evolution and relationship between species within one family of bacteria.”

More information is available in the full report now published in the Proceedings of the National Academy of Sciences