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Borrelia burgdorferi , the causative agent of Lyme disease in the United States, is able to persist in the joint, heart, skin, and central nervous system for the lifetime of its mammalian host.Borrelia species achieve dissemination to distal sites in part by entry into and travel within the bloodstream. Much work has been performedin vitro describing the roles of manyB. burgdorferi outer surface proteins in adhesion to host cell surface proteins and extracellular matrix components, although the biological relevance of these interactions is only beginning to be exploredin vivo . A need exists in the field for anin vivo model to define the biological roles ofB. burgdorferi adhesins in tissue-specific vascular interactions. We have developed anin vivo model of vascular interaction ofB. burgdorferi in which the bacteria are injected intravenously and allowed to circulate for 1 h. This model has shown that the fibronectin binding protein BB0347 has a tropism for joint tissue. We also have shown an importance of the integrin binding protein, P66, in binding to vasculature of the ear and heart. This model also revealed unexpected roles forBorrelia adhesins BBK32 and OspC in bacterial burdens in the bloodstream. The intravenous inoculation model of short-term infection provides new insights into criticalB. burgdorferi interactions with the host required for initial survival and tissue colonization.

A Short-Term Borrelia burgdorferi Infection Model Identifies Tissue Tropisms and Bloodstream Survival Conferred by Adhesion Proteins