Single Gene Leap Led to Flea Transmission of Plague

Their findings were reported in the April 25, 2002, issue of Science.

By acquiring this gene, the bacterium gradually changed from a germ that caused a mild human stomach illness acquired from contaminated food or water to the flea-borne agent of the Black Death, which in the 14th century killed one-fourth of Europe's population.

Our research illustrates how a single genetic change can profoundly affect the evolution of disease. In this case, that genetic change set the stage for a completely new route of
disease transmission, notes B. Joseph Hinnebusch, Ph.D., lead author of the study and plague expert at Rocky Mountain Laboratories, a Montana (USA) outpost of the US National Institute of Allergy and Infectious Diseases (NIAID).

The gene allowed the bacteria to be transmitted through the bite of an insect--in this case, the flea--an adaptation that distinguishes Yersinia pestis, the plague germ, from closely related, more benign gut bacteria. In turn, as Y pestis adapted to rely on its new blood-feeding host for transmission, the emergence of more deadly bacterial strains would have been favored, the researchers conclude.

In the report, Dr. Hinnebusch and colleagues from Sweden, Michigan, and NIAID describe how they explored the source of this gene. The gene codes for an enzyme known as PLD. Previous work indicated that Y pestis picked up this gene from either an unrelated bacterium or a simple nucleated organism. The researchers infected fleas with variants of Y pestis that either contained or lacked the PLD gene and then observed the outcome. They discovered that the enzyme is required for survival of the plague bacterium in the midgut of the rat flea. Although the enzyme's activity protects Y pestis from being destroyed, the researchers do not yet know the molecular mechanism by which this protection occurs. To find that out is clearly the next step, Dr. Hinnebusch notes.
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