Plague bug not so fierce after all

DNA analysis shows bacterium was fairly ordinary but thrived in pestilent conditions of medieval Europe

Using methods that seem inspired by Frankenstein and Jurassic Park, scientists have reconstructed the entire DNA sequence of the ancient microbe responsible for the Black Death, the plague that killed half of Europe’s population between 1347 and 1351.

BLACK DEATH BONES The skeletal remains of medieval plague victims exhumed from the East Smithfield cemetery by the Museum of London Archaeology have helped scientists reconstruct the genetic code of Yersinia pestis, the microbe that caused the Black Death. © Museum of London Archaeology

Using bits of the bacterium Yersinia pestis plucked from the teeth of four well-preserved skeletons of plague victims excavated from London’s East Smithfield cemetery in the 1980s, an international team of researchers found that the medieval microbe has nearly the same genetic code as modern strains of the bacterium. The scientists found no evidence that genetic mutations helped the 14th century strain of Y. pestis notch such a massive death toll.

“As to why this killed so many people across Europe in 1348, there is no particular smoking gun,” says geneticist Hendrik Poinar of McMaster University in Ontario, Canada, a member of the international team of anthropologists and evolutionary geneticists who published their findings online October 12 in Nature.

Instead, a variety of non-genetic factors that are difficult to control most likely helped the infectious disease spread and made it more lethal. “The climate was beginning to dip,” says Poinar. “It got very cold, very wet very quickly.”

More rain meant less food for people who were already poorly nourished. Crowded cities also played host to millions of rats, which provided the fleas that carry Y. pestis a warm — and mobile — home. Weakened by hunger and stressful living conditions, medieval Europeans’ immune systems weren’t prepared to fight off the rodent-borne pathogen.

Though genetically similar to its ancestor, the modern strain of Y. pestis sticks almost exclusively to rodents and has trouble jumping from human to human. Antibiotics and other advances of modern medicine may have eliminated the need for a pied piper, but in the age of the bird flu and other animal-carried diseases, puzzling out why humans proved so susceptible to the ancient strain of Yersinia pestis is still important, researchers say.

Reconstructing genetic information about pathogens such as Y. pestis will play an important role in revealing the character of other kinds of infectious diseases, says Samuel Cohn of the University of Glasgow in Scotland. He notes, however, that understanding how a particular disease affects people takes more than knowledge of the microbe that causes it.  “A disease is a relationship between a pathogen and its host, and that relationship changes over time,” he says.

If that relationship happens to change again, and a pathogen dumps its animal host for a human body, Poinar says his team’s method of ancient DNA sequencing may help public officials stave off future pandemics by helping them predict how a life-threatening microbe will interact with the human immune system, treatments and even other microbes.

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