Biology of infection with Borrelia burgdorferi

Abstract

The spirochete Borrelia burgdorferi is a tick-borne obligate parasite whose normal reservoir is a variety of small mammals. Although infection of these natural hosts does not lead to disease, infection of humans can result in Lyme disease as a consequence of the human immunopathologic response to B burgdorferi. Consistent with the pathogenesis of Lyme disease, bacterial products that allow B burgdorferi to replicate and survive seem to be primarily what is required for the bacterium to cause disease in a susceptible host. This article describes the basic biology of B burgdorferi and reviews some of the bacterial components required for infection of and survival in the mammalian and tick hosts.

Fig. 1

B. burgdorferi outer surface proteins are differentially regulated in response to host conditions. Spirochetes remodel their outer surface in different host environments, represented above by different colors. In the unfed tick, B. burgdorferi (represented in blue) produce a variety of proteins, such as OspA, to persist within the tick midgut for extended periods of time. Once a tick has attached to a vertebrate host, B. burgdorferi (now represented in red) expresses other proteins (e.g. OspC) in preparation for transmission to the new host. During infection of the mammalian host, B. burgdorferi (colored in yellow) expresses a variety of other proteins (including VlsE), presumably to survive attack by the host immune system, disseminate to distant sites within the host, and acquire specific nutrients. This figure shows representative proteins and is not meant to be a comprehensive list.