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Infection and Immunity, June 2006, p. 3678-3681, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.00043-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Infectivity of the Highly Transformable BBE02– lp56– Mutant of Borrelia burgdorferi, the Lyme Disease Spirochete, via Ticks

Mary B. Jacobs,1 Steven J. Norris,2 Kathrine M. Phillippi-Falkenstein,3 and Mario T. Philipp1*

Divisions of Bacteriology and Parasitology,1 Veterinary Medicine, Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana 70433,3 Department of Pathology and Laboratory Medicine and Department of Microbiology and Molecular Genetics, University of Texas Medical School at Houston, Houston, Texas 770302

Received 9 January 2006/ Returned for modification 10 February 2006/ Accepted 28 March 2006

Infectious Borrelia burgdorferi strains that have increased transformability with the shuttle vector pBSV2 were recently constructed by inactivating the gene encoding BBE02, a putative restriction-modification gene product expressed by the linear plasmid lp25 (Kawabata et al., Infect. Immun. 72:7147-7154, 2004). The absence of the linear plasmid lp56, which carries another putative restriction-modification gene, further enhanced transformation rates. The infectivity of these mutants was assessed previously in mice that were inoculated with needle and syringe and was found to be equivalent to that of wild-type spirochetes. Here we examined the infectivity of spirochetes to ticks after capillary inoculation of Ixodes scapularis nymphs and the subsequent spirochetal infectivity to mice via ticks by using B. burgdorferi B31 clonal isolates lacking lp56 and/or BBE02. The absence of lp56 (but not BBE02) correlated with a lower number of spirochetes in ticks after feeding on mice; this plasmid thus may play a role, albeit not an essential one, in supporting spirochetal survival in the feeding tick. Importantly, however, the absence of lp56 and BBE02 did not detectably influence infectivity to mice via ticks.

* Corresponding author. Mailing address: Tulane National Primate Research Center, Tulane University Health Sciences Center, 18703 Three Rivers Rd., Covington, LA 70433. Phone: (985) 871-6221. Fax: (985) 871-6390. E-mail: philipp{at}tpc.tulane.edu.

Editor: V. J. DiRita

Infection and Immunity, June 2006, p. 3678-3681, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.00043-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Stewart, P. E., Bestor, A., Cullen, J. N., Rosa, P. A. (2008). A Tightly Regulated Surface Protein of Borrelia burgdorferi Is Not Essential to the Mouse-Tick Infectious Cycle. Infect. Immun. 76: 1970-1978 [Abstract] [Full Text]  


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