Sultan SZ, Manne A, Stewart PE, Bestor A, Rosa PA, Charon NW, Motaleb MA. Infection and Immunity, online before print, 2013 Mar 25.
The Lyme disease spirochete, Borrelia burgdorferi, exists in a zoonotic cycle involving an arthropod tick and mammalian host. Dissemination of the organism within and between these hosts depends upon the spirochete’s ability to traverse through complex tissues. Additionally, the spirochete outruns the host immune cells while migrating through the dermis, suggesting the importance of B. burgdorferi motility in evading host clearance. B. burgdorferi’s periplasmic flagellar filaments are composed primarily of a major protein, FlaB and minor protein, FlaA. By constructing a flaB mutant that is non-motile, we investigated for the first time the absolute requirement for motility in the mouse-tick life cycle of B. burgdorferi. We found that whereas wild-type cells are motile and have a flat-wave morphology, mutant cells were non-motile and rod-shaped. These mutants were unable to establish infection in C3H/HeN mice via both needle injection and tick bite. In addition, these mutants had decreased viability in fed ticks. Our studies provide substantial evidence that the periplasmic flagella, and consequently motility, are critical not only for optimal survival in ticks, but also for infection of the mammalian host by the arthropod tick vector.