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Of the 31 validated species in the genus Bartonella, 11 are agents of serious infectious diseases of humans, among them Carrión’s disease, trench fever, cat-scratch disease, and bacillary angiomatosis. Bartonella are extremely widespread, having been found in virtually every type of mammal surveyed. As facultative intracellular parasites employing hemotrophy (infection of red blood cells), the key to their success comes in their ability to survive within the bloodstream of their host or reservoir. It has been demonstrated that bartonellae are resistant to the effects of complement proteins in serum, the primary agents of the innate immune system. Although this effect has been repeatedly observed, the molecular basis of Bartonella’s resistance remains undetermined. The overall objective of this research is to examine the genetic and molecular components of complement resistance in bartonellae using Bartonella bacilliformis (Bb) as a model species. In order to address our hypothesis that complement resistance has a genetic basis and likely encodes a surface-exposed protein or component of the bacterium, we had three original experimental aims. In aim 1, we planned to use the Himar1 transposon to generate a signature-tagged mutagenesis (STM) library of Bb. In aim 2, we were to screen the library to identify the specific gene(s) involved with serum complement resistance. In aim 3, we were going to analyze the gene(s) that confer this resistance by automated DNA sequencing and genetic manipulation. The results of this study would allow us to analyze complement resistance in Bartonella and increase our understanding of complement resistance in other pathogenic bacteria.