Deadly Pickup: Enzyme permits plague germ to ride in fleas
By John Travis
Acquisition of a gene that enables the plague bacterium to live inside bloodsucking fleas may have set the stage for the Black Death, a new study in the April 26 Science suggests. This plague epidemic killed an estimated 25 million people during medieval times.
“It’s sobering to think about. An organism can pick up one or two [genes] and be capable of producing a new pandemic,” says study coauthor B. Joseph Hinnebusch of the National Institute of Allergy and Infectious Diseases in Hamilton, Mont.
Discovered several decades ago in the plague bacterium, Yersinia pestis, the crucial gene encodes an enzyme that cleaves molecules known as phospholipids. The enzyme originally earned the name Yersinia murine toxin (Ymt) because extracts containing the molecule were toxic to mice and other animals.
That made sense given the life cycle of Y. pestis. The plague bacterium infects and causes disease in rodents. Blood-eating fleas that tap into these rodents can then pass the microbes on to other hosts, including people.
Recently, however, ke Forsberg of Ume University in Sweden noticed that the gene for Ymt was much more active in Y. pestis growing at 26C than at 37C, the body temperature of mice. This, and subsequent mouse studies, indicated that Y. pestis might use this gene more in the flea stage of the microbe’s life cycle rather than in its rodent stage.
Working with Forsberg, Hinnebusch and his colleagues have now confirmed this hypothesis. Fleas infected with Y. pestis strains containing mutations in the Ymt gene rarely transmitted the bacterium in their bites. Further study showed that such microbes fail to colonize the fleas’ midguts, indicating that Ymt normally protects the germ from an antimicrobial substance there.
Moreover, after the researchers added the Ymt gene to other bacteria, including one called Yersinia pseudotuberculosis, the microbes were much better able to persist in the flea midgut. The plague bacterium is thought to have evolved relatively recently from Y. pseudotuberculosis by acquiring genes from other microbes (SN: 11/27/99, p. 343).
“This is one of the first papers that deals with what it takes [for the plague bacterium] to survive and grow in the flea,” says Robert Perry of the University of Kentucky College of Medicine in Lexington.