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Infection and Immunity, July 2009, p. 2672-2682, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.01193-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

OspC-Independent Infection and Dissemination by Host-Adapted Borrelia burgdorferi{triangledown}

Kit Tilly,* Aaron Bestor, Daniel P. Dulebohn, and Patricia A. Rosa

Laboratory of Zoonotic Pathogens, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, Montana 59840

Received 25 September 2008/ Returned for modification 4 November 2008/ Accepted 20 April 2009

Borrelia burgdorferi OspC is required for the spirochete to establish infection in a mammal by tick transmission or needle inoculation. After a brief essential period, the protein no longer is required and the gene can be shut off. Using a system in which spirochetes contain only an unstable wild-type copy of the ospC gene, we can obtain mice persistently infected with bacteria lacking OspC. We implanted pieces of infected mouse skin subcutaneously in naïve mice, using donors carrying wild-type or ospC mutant spirochetes, and found that both could infect mice by this method, with similar numbers of wild-type or ospC mutant spirochetes disseminated throughout the tissues of recipient mice. Recipient mouse immune responses to tissue transfer-mediated infection with wild-type or ospC mutant spirochetes were similar. These experiments demonstrate that mammalian host-adapted spirochetes can infect and disseminate in mice in the absence of OspC, thereby circumventing this hallmark of tick-derived or in vitro-grown spirochetes. We propose a model in which OspC is one of a succession of functionally equivalent, essential proteins that are synthesized at different stages of mammalian infection. In this model, another protein uniquely present on host-adapted spirochetes performs the same essential function initially fulfilled by OspC. The strict temporal control of B. burgdorferi outer surface protein gene expression may reflect immunological constraints rather than distinct functions.

* Corresponding author. Mailing address: 903 S. 4th Street, Hamilton, MT 59840. Phone: (406) 375-7466. Fax: (406) 363-9681. E-mail: ktilly{at}niaid.nih.gov

{triangledown} Published ahead of print on 27 April 2009.

Editor: J. B. Bliska

Infection and Immunity, July 2009, p. 2672-2682, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.01193-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Sarkar, A., Tilly, K., Stewart, P., Bestor, A., Battisti, J. M., Rosa, P. A. (2009). Borrelia burgdorferi Resistance to a Major Skin Antimicrobial Peptide Is Independent of Outer Surface Lipoprotein Content. Antimicrob. Agents Chemother. 53: 4490-4494 [Abstract] [Full Text]  


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