The Lyme disease spirochetes, Borrelia burgdorferi (sensu lato), must cause persistent, disseminated infection to be maintained in the natural enzootic cycle. In human Lyme disease, spirochetes spread from the site of a tick bite to colonize multiple tissue sites, causing multisystem clinical manifestations. The Lyme spirochetes produce many adhesive surface proteins that collectively recognize diverse host substrates and cell types and are likely to promote dissemination and chronic infection in a variety of tissues. Recent application of state-of-the-art in vivo imaging technologies is illuminating mechanisms of interaction of B. burgdorferi with the host and the importance of multiple adhesins during mammalian infection.
Keywords: Borrelia burgdorferi; Lyme disease; adhesins; dissemination; intravital imaging; transmigration.
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