The bacterium that causes leprosy still packs the same punch it did in the Middle Ages, a study of the organism’s genome reveals.
Mycobacterium leprae causes skin sores, nerve damage and skeletal disfigurement. About 200,000 people worldwide contract leprosy each year. In early medieval Europe the bacterial infection was more common, but its incidence began to wane in the 16th century.
M. leprae has a bare-bones genome that doesn’t allow the microbe to survive outside a human or animal host. About half of the organism’s genes have been disabled and no longer make proteins. Many scientists thought this genome decay contributed to the disease’s decline in prevalence, says Patrick Brennan, a microbiologist at Colorado State University in Fort Collins.
Hoping to find the genetic changes that led to leprosy’s decline, an international group of researchers extracted bacterial DNA from 24 skeletons of leprosy victims from 10th- to 17th-century Sweden, Denmark and England. One sample was so well preserved that the researchers were able to reconstruct the medieval bacterium’s entire genome.
The team then compared the medieval bacterium’s genome to those of bacteria isolated from leprosy patients living in India, Thailand, the United States and Brazil. “We could find no meaningful differences,” says coauthor Stewart Cole of the Swiss Federal Institute of Technology in Lausanne. The team reports the finding June 13 in Science.
The bacterium’s genetic stability may be due to its stripped-down genome, says Helen Donoghue, of University College London, who has studied ancient leprosy strains. “There’s not a lot of scope for further change,” she says.
Given that leprosy hasn’t changed much in a millennium, Cole and his coauthors speculate that leprosy’s exit from the European stage was due to the social isolation of people with leprosy and the rise of other diseases, such as the plague and tuberculosis.