That proportion of defunct code is among the highest detected in a micro-organism and helps explain why the leprosy pathogen has one of the slowest generation times of its unicellular kind, dividing just once every 12 to 14 days, against 20 minutes for the ubiquitous E. coli.

Some researchers attribute the microbe’s decayed genome to its prolonged and virtually exclusive relationship with its human host.

“It’s reductive evolution,” said Erwin Schurr, a molecular geneticist at McGill University — a swapping of plasticity in favor of specialization and a degree of complacency.

Dr. Xiang Y. Han of the University of Texas M. D. Anderson Cancer Center said the pseudogenes were a result of a “chase-hide” game, with the microbial “mouse” gradually shedding as many surface proteins as possible to elude our prowling cat of an immune system.

Slow-growing though the bacteria may be, if left untreated, they will multiply into the many trillions, forming thick, scaly nodules on the face and extremities — “lepra” is the Greek word for scaly — and destroying the Schwann cells that sheathe and protect the nerves of the peripheral nervous system.

Reporting recently in the journal PLOS Neglected Tropical Diseases, Dr. Han and Francisco J. Silva of the University of Valencia in Spain sought to trace the antiquity of leprosy by comparing the genomes of M. leprae and a closely related pathogen named Mycobacterium lepromatosis, which Dr. Han recently discovered. The researchers hypothesize that the common ancestor of the two leprosy microbes jumped into our pre-hominid forebears in Africa some 10 million years ago and migrated with us as we colonized the world.

Today, Hansen’s is classified as a rare disease, yet it still strikes some 200,000 people a year, most of them in Brazil, India and other developing nations.