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Key to Lyme Disease Virulence Discovered

Protein helps transport manganese in the bacteria behind the disease, study finds


WEDNESDAY, Feb. 11 (HealthDay News) -- A protein that's essential for the bacterium that causes Lyme disease to become virulent has been identified by microbiologists at the University of Texas Southwestern Medical Center at Dallas.

The researchers said their finding may help lead to new methods of fighting the tick-borne infection.

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This bacterial protein, called BmtA, aids in transporting the metal manganese from a host tick or mammal to the Lyme-disease causing bacterium Borrelia burgdorferi.

In this study, the researchers examined the effect that B. burgdorferi genetically engineered to lack BmtA had on mice. In a test tube, the altered bacteria grows more slowly but isn't dramatically different from the normal version.

"When you try to grow it in a mouse, however, it can't grow," senior study author Dr. Michael Norgard, chairman of microbiology at UT Southwestern, said in a university news release. "The fact that the bacterium without this particular manganese transporter can't grow in a mouse raises important questions about what aspects of physiology and metabolism contribute to the pathogenicity of the organism."

The researchers also learned that B. burgdorferi doesn't seem to require iron to function.

"Out of the thousands of bacteria known, the Lyme disease agent and only one or two other bacterial species do not require iron for growth," lead author Dr. Zhiming Ouyang, a postdoctoral researcher in microbiology, said in the news release. "That raises the question as to what other metal co-factors the Lyme disease bacterium depends on to carry out the work that iron does for all these other biological systems. Our research suggests that manganese is a really important one."

The study was published in this week's online issue of the Proceedings of the National Academy of Sciences.

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-- Robert Preidt

Copyright © 2009 ScoutNews, LLC. All rights reserved.
Last updated 2/11/2009

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SOURCE: University of Texas Southwestern Medical Center at Dallas, news release, Feb. 9, 2009


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