The laboratory mouse model of
Lyme disease has revealed that Borrelia burgdorferi differentially expresses numerous outer
surface proteins that influence different stages of
infection (tick-borne transmission, tissue colonization, dissemination, persistence, and tick acquisition). Deletion of two such outer
surface proteins,
decorin-
binding proteins A and B (
DbpA/B), has been documented to decrease infectivity, impede early dissemination, and, possibly, prevent persistence. In this study,
DbpA/B-deficient spirochetes were confirmed to exhibit an early dissemination defect in immunocompetent, but not immunodeficient, mice, and the defect was found to resolve with chronicity. Development of disease (
arthritis and
carditis) was attenuated only in the early stage of
infection with
DbpA/B-deficient spirochetes in both types of mice. Persistence of the
DbpA/B-deficient spirochetes occurred in both immunocompetent and immunodeficient mice in a manner indistinguishable from that of wild-type spirochetes. Dissemination through the lymphatic system was evaluated as an underlying mechanism for the early dissemination defect. At 12 h, 3 days, 7 days, and 14 days postinoculation,
DbpA/B-deficient spirochetes were significantly less prevalent and in lower numbers in lymph nodes than wild-type spirochetes. However, in immunodeficient mice, deficiency of
DbpA/B did not significantly decrease the prevalence or spirochete numbers in lymph nodes. Complementation of
DbpA/B restored a wild-type phenotype. Thus, the results indicated that deficiency of
DbpA/B allows the acquired immune response to restrict early dissemination of spirochetes, which appears to be at least partially mediated through the lymphatic system.