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In order to elucidate the immune evasion mechanisms of<jats:italic>B. spielmanii<\/jats:italic>, we compared the abilities of isolates obtained from Lyme disease patients and tick isolate PC-Eq17 to escape from complement-mediated bacteriolysis. Using a growth inhibition assay, we show that four<jats:italic>B. spielmanii<\/jats:italic>isolates, including PC-Eq17, are serum resistant, whereas a single isolate, PMew, was more sensitive to complement-mediated lysis. All isolates activated complement in vitro, as demonstrated by covalent attachment of C3 fragments; however, deposition of the later activation products C6 and C5b-9 was restricted to the moderately serum-resistant isolate PMew and the serum-sensitive<jats:italic>B. garinii<\/jats:italic>isolate G1. Furthermore, serum adsorption experiments revealed that all<jats:italic>B. spielmanii<\/jats:italic>isolates acquired the host alternative pathway regulators factor H and factor H-like protein (FHL-1) from human serum. Both complement regulators retained their factor I-mediated C3b inactivation activities when bound to spirochetes. In addition, two distinct factor H and FHL-1 binding proteins, BsCRASP-1 and BsCRASP-2, were identified, which we estimated to be approximately 23 to 25 kDa in mass. A further factor H binding protein, BsCRASP-3, was found exclusively in the tick isolate, PC-Eq17. This is the first report describing an immune evasion mechanism utilized by<jats:italic>B. spielmanii<\/jats:italic>sp. nov., and it demonstrates the capture of human immune regulators to resist complement-mediated killing.<\/jats:p>","DOI":"10.1128\/iai.00532-07","type":"journal-article","created":{"date-parts":[[2007,7,17]],"date-time":"2007-07-17T00:40:32Z","timestamp":1184632832000},"page":"4817-4825","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":44,"title":["Human Pathogenic<i>Borrelia spielmanii<\/i>sp. nov. 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