The closest many of us in the developed world get to leprosy these days might be a viewing of Ben Hur or the Life of Brian. But the disease isn’t confined to the history books and still affects up to a quarter of a million people every year. In 2011, there were nearly 220,000 new cases of leprosy reported worldwide.

And looking through the lens of history, a group of researchers has found that the bacteria that cause leprosy have hardly changed in 1000 years. Using bacteria found in five medieval skeletons excavated in Sweden, Denmark and Winchester in the UK, the researchers were able to reconstruct the genomes of a sample of bacteria and compare them to their modern-day counterparts - taken from biopsies of people with the disease today.

The genome sequences from the medieval skeletons were then compared to 11 modern strains of the disease. And they found that all leprosy bacteria in the last 4,000 years share a common ancestor. The earliest skeletal evidence found for the disease dates back to 2000 BC in India.

It’s the first time that such detailed information on the origins and evolution of the bacteria has been revealed.

Leprosy is a disease caused by the Mycobacterium leprae bacterium which attack the nerves in the body’s extremities. Symptoms can include paler patches and lumps on the skin, as well as a loss of feeling and muscle weakness, caused by thickened nerves. Leprosy sufferers are prone to sustaining terrible injuries to their hands and feet, because they cannot feel them.

The disease was a common problem in the UK and Europe during the Middle Ages - some one in 30 people are estimated to have been affected - but by the 16th century the disease had receded.

The findings raise a huge number of questions about the disease which we still don’t have the answers to - such as why it still persists in the 21st century.

Dr Graham Stewart, Professor of Molecular Bacteriology at the University of Surrey and co-author of the study, said this is still something of a mystery. “There is a definite possibility that leprosy could be eliminated in the future,” he said. “But progress seems to be surprisingly slow.”

Although some modern strains of the disease show resistance to Dapsone, one of the components of Multi-Drug Therapy - the treatment generally used to treat the disease - Stewart said this wasn’t a widespread problem because leprosy grows slowly, only replicating once every two weeks.

“We know that the bacteria can persist in protozoa like amoebae and possibly insects, so these may still be sources of the disease,” Dr Helen Donoghue, from University College London said.

Despite its persistence, huge progress has been made against the disease since the Middle Ages. This could be for a number of reasons. Dr Stewart Cole, Professor at the École Polytechnique Fédérale de Lausanne and another co-author of the study, said there was some indication that some populations evolved to be more resistant to the disease. “If the explanation of the drop in leprosy cases isn’t in the pathogen, then it must be in the host, that is, in us,” he said.

Stewart corroborated this. He said genetic markers for resistance to leprosy are frequently found in modern Europeans.

There appears to be more to the story, though. “Human genetics influences susceptibility to leprosy to some extent,” Donoghue said. “Better nutrition and better housing are also possible reasons for the overall decline.” In a paper she wrote, Donoghue suggested that the migration from country to city following the Black Death, which is believed to have wiped out millions of Europe’s population, led to the decline of leprosy in Western Europe.

This is because higher population density resulted in the spread of tuberculosis, which kills much faster than leprosy. “It is possible to find archaeological cases of leprosy where Mycobacterium tuberculosis DNA is present as well,” explained Donoghue.

There is plenty left to discover about both the history of leprosy. “A great experiment would be to look at people who suffered from Leprosy in the Middle Ages, and sequence the DNA of these hosts so we could see how it compares to our own,” Stewart said.

Another idea involves sequencing the genome of Mycobacterium lepromatosis, a close cousin to Mycobacterium leprae. “This could fill in a number of unknowns about the evolutionary history of leprosy,” Stewart said. It would also be possible to extend the research to further study the plague and tuberculosis, Steward added.

Despite remaining unchanged for hundreds of years, leprosy still keeps many of its secrets under wraps.