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Infection and Immunity, August 2003, p. 4608-4613, Vol. 71, No. 8
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.8.4608-4613.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The Absence of Linear Plasmid 25 or 28-1 of Borrelia burgdorferi Dramatically Alters the Kinetics of Experimental Infection via Distinct Mechanisms

Maria Labandeira-Rey, J. Seshu, and Jonathan T. Skare*

Department of Medical Microbiology and Immunology, The Texas A&M University System Health Science Center, College Station, Texas 77843-1114

Received 14 March 2003/ Returned for modification 22 April 2003/ Accepted 8 May 2003

The 25-kb linear plasmid lp25 and one of the 28-kb linear plasmids (lp28-1) are required for experimental infection in Borrelia burgdorferi, the etiologic agent of Lyme disease. The loss of these plasmids either eliminates infectivity (lp25) or significantly increases the 50% infective dose during a 2-week infection period (lp28-1). This study assessed the kinetics of bacterial dissemination in C3H/HeN mice infected with B. burgdorferi lacking either lp25 or lp28-1, as well as their wild-type parent, and tracked the development of specific borrelial antibodies over a 3-week period. The results indicated that the wild type and the lp28-1- strains were able to disseminate throughout the host, whereas the lp25- strain was cleared within 48 h of inoculation. While the wild-type B. burgdorferi persisted in tissues for the duration of the study, the lp28-1- mutant began clearing at day 8, with no detectable bacteria present by day 18. As expected, the wild-type strain persisted in C3H/HeN mice despite a strong humoral response; however, the lp28-1- mutant was cleared coincidently with the development of a modest immunoglobulin M response. The lp28-1- mutant was able to disseminate and persist in C3H-scid mice at a level indistinguishable from that of wild-type cells, confirming that acquired immunity was required for clearance in C3H/HeN mice. Thus, within an immunocompetent host, lp28-1-encoded proteins are not required for dissemination but are essential for persistence associated with Lyme borreliosis.

* Corresponding author. Mailing address: 407 Reynolds Medical Building, Department of Medical Microbiology and Immunology, The Texas A&M University System Health Science Center, College Station, TX 77843-1114. Phone: (979) 845-1376. Fax: (979) 845-3479. E-mail: jskare{at}tamu.edu.

Editor: D. L. Burns

Infection and Immunity, August 2003, p. 4608-4613, Vol. 71, No. 8
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.8.4608-4613.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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