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National Institute of Allergy and
Infectious Diseases (NIAID)
http://www.niaid.nih.gov

FOR IMMEDIATE RELEASE
Thursday, April 25, 2002

Media Contact:
Laurie K. Doepel
(301) 402-1663
niaidnews@niaid.nih.gov
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Single Gene Leap Led to Flea-Borne Transmission of Plague Bacterium

A single gene change in a relatively benign recent ancestor of the bacterium that causes bubonic plague played a key role in the evolution of the deadly disease, researchers report in the April 25 issue of the journal Science. By acquiring this gene, the bacterium gradually changed from a germ that causes a mild human stomach illness acquired via 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.

The new research adds an important piece to understanding the forces behind the emergence of plague, which occurred within the past 1,500 to 20,000 years. "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 in Rocky Mountain Laboratories, a Montana outpost of the 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 all 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.

The evolution of the plague bacterium is just one example of how microbes persistently challenge researchers by unexpectedly repackaging themselves, in any of multiple ways, to emerge as novel or more virulent agents of human disease.

In the new report, Dr. Hinnebusch and his colleagues from Sweden, Michigan, and NIAID describe how they explored the source of this gene and later identified the critical role it plays.

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.

Next 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, thereby allowing it to colonize the flea gut freely, 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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References:


BJ Hinnebusch, AE Rudolph, P Cherepanov, JE Dixon, TG Schwan, and A Forsberg. Role of Yersinia murine toxin in survival of Yersinia pestis in the midgut of the flea vector. Science 296:733-35 (2002).

Press releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.


NIAID conducts and supports research—at NIH, throughout the United States, and worldwide—to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at www.niaid.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

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Last Updated April 25, 2002