It is an infectious disease that dates back at least to biblical times, yet leprosy has puzzled scientists since the identification, in 1873, of the bacterium that causes it.
Known for its disfiguring skin lesions and potentially debilitating nerve damage, leprosy, or Hansen's disease, is a very difficult disease to transmit. It also has a long incubation period, making it hard for a doctor to determine where a leprosy patient contracted the disease.
But now a team of French scientists has discovered how the disease evolved and how it was spread across the continents by human migrations.
The scientists found that leprosy infections were caused by a single bacterial clone, which spread—but barely mutated—for centuries. Such behavior is highly unusual.
Researchers also found that leprosy probably originated in East Africa and not India, as previously thought. The disease was brought eastward and westward by colonialism and the slave trade, the scientists believe.
"The bacterium has a highly stable genome and appears to have been spread between people by contact or the aerosol [airborne particles] route and dispersed around the world by human migrations," said Stewart Cole, a geneticist at the Pasteur Institute in Paris, France.
Cole is a co-author of the study, which is reported this week in the academic journal Science.
Slow Incubation
For centuries leprosy was incurable and severely disfiguring. Lepers were usually shunned and sequestered in leper colonies.
The disease produces lesions on the skin. The most severe form of leprosy produces large disfiguring nodules, or lumps. The disease can also cause nerve damage in the extremities, sensory loss in the skin, and muscle weakness.
Although leprosy is easily curable by antibiotic therapy today, the disease is still common in many countries in the world, especially in tropical climates. About a hundred cases per year are diagnosed in the United States. An unusual aspect of leprosy infection is the disease's slow incubation period, which lasts several years.
The bacterium is very difficult to study. Its genome is filled with damaged, nonfunctional genes, which may explain why it grows so slowly.
Apart from humans, it afflicts only armadillos and the footpads of mice. Scientists cannot grow the bacterium in the laboratory.
"Even if we could grow it on petri dishes, it would take 9 to 12 months to form a colony," Cole said.
So instead Cole and his colleagues compared the genomes of seven strains of the bacterium taken from leprosy patients around the world. The scientists found very little variations between the strains. This, they say, suggests that there was a single clone at the origin of all cases of leprosy.
"Their analysis … appears to explain some of what we know about the disease leprosy and the [source] organism that causes leprosy, namely the slow growth of the organism and progression of the disease," said Kenrad Nelson. Nelson is an epidemiologist and leprosy expert at Johns Hopkins University in Baltimore, Maryland, and was not involved in the research.
Slave Trade
By analyzing very rare mutations in individual molecules in the bacterium, the scientists were able to trace how the disease spread over the course of human history.
"By comparing the evolutionary scheme for [the bacterium] with the map of known human migrations, we found some striking parallels and differences," Cole said.
Researchers previously believed that leprosy originated on the Indian subcontinent before being introduced to Europe by Greek soldiers returning from the India campaign of Alexander the Great.
The new findings, however, indicate that the disease actually originated in East Africa—or perhaps the Middle East.
The scientists say Europeans and North Africans spread the disease to West Africa. From there the slave trade brought it to the Caribbean, South America, and North America.
Colonialism played a major part in the spread of leprosy, Cole said. "It is clear that Europeans introduced the disease to the Americas themselves and by slavery. Other human migrations in history almost certainly did the same thing."
Erwin Schurr, a researcher at McGill University's Centre for the Study of Host Resistance in Montreal, Canada, said the new study's insights into leprosy's natural history were "extremely exciting."
The results "provide critically important clues for an understanding of host-pathogen interaction in leprosy," he said. "Moreover, it will be highly interesting to contrast these findings with similar studies in tuberculosis that suggest a more genetically diverse pathogen pool." |