Infect Immun. 2014 Sep 22. pii: IAI.02613-14. [Epub ahead of print]
pncA and bptA are not sufficient to complement Ixodes colonization and persistence by B. burgdorferi in lp25 deficient background.
The complex segmented genome of Borrelia burgdorferi is comprised of a linear chromosome along with numerous linear and circular plasmids essential for tick and/or mammalian infectivity. The pathogenic necessity for specific borrelial plasmids has been identified; most notably, infection of the tick vector and mammalian host both require linear plasmid 25 (lp25). Genes encoded on lp25, specifically bptA and pncA, are postulated to play a role for B. burgdorferi to infect and persist in Ixodes ticks. In this study, we complemented an lp25 deficient borrelial strain with pncA or pncA accompanied by bptA to evaluate their ability to restore larval colonization and persistence through transstadial transmission relative to wild type B. burgdorferi. The acquisition and/or survival of the complemented strains by larvae from infected mice was significantly decreased when assayed by cultivation and qPCR. Only 10% of the pncA complemented strain were found by culture to survive 17 days following larval feeding, while 45% of the pncA/bptA complemented strain survived, with similar results by PCR. However, neither of the complemented B. burgdorferi strains were capable of persisting through the molt to the nymphal stage as analyzed by culture. qPCR analyses of unfed nymphs detected B. burgdorferi genomes in several nymphs at low copy numbers, likely indicating the presence of DNA from dead or dying cells. Overall, the data indicates that pncA and bptA cannot independently support infection suggesting that lp25 encodes additional gene(s) or regulatory elements critical for B. burgdorferi survival and pathogenesis in the Ixodes vector.
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