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Borrelia burgdorferi , the causative agent of Lyme borreliosis, is transmitted to humans from the bite of  Ixodes  spp. ticks. During the borrelial tick-to-mammal life cycle,  B. burgdorferi  must adapt to many environmental changes by regulating several genes, including  bba64 . Our laboratory recently demonstrated that the  bba64  gene product is necessary for mouse infectivity when  B. burgdorferi  is transmitted by an infected tick bite, but not via needle inoculation. In this study we investigated the phenotypic properties of a  bba64  mutant strain, including 1) replication during tick engorgement, 2) migration into the nymphal salivary glands, 3) host transmission, and 4) susceptibility to the MyD88-dependent innate immune response. Results revealed that the  bba64  mutant's attenuated infectivity by tick bite was not due to a growth defect inside an actively feeding nymphal tick, or failure to invade the salivary glands. These findings suggested there was either a lack of spirochete transmission to the host dermis or increased susceptibility to the host's innate immune response. Further experiments showed the  bba64  mutant was not culturable from mouse skin taken at the nymphal bite site and was unable to establish infection in MyD88-deficient mice via tick infestation. Collectively, the results of this study indicate that BBA64 functions at the salivary gland-to-host delivery interface of vector transmission and is not involved in resistance to MyD88-mediated innate immunity.

Functional Analysis of the Borrelia burgdorferi bba64 Gene Product in Murine Infection via Tick Infestation