Spread of bacteria via the bloodstream to vital organs causes most mortality due to bacterial infection. To exit the bloodstream and enter these organs, bacteria must be able to resist the forces generated by flowing blood so that they can adhere to the endothelial cells lining blood vessels without being washed away. This process is not yet understood for most disease-causing bacteria. Here, we show that the Lyme disease pathogen Borrelia burgdorferi exploits an abundant constituent of blood, plasma fibronectin, to form endothelial interactions that become stronger as forces due to blood-flow increase. The ability to recruit this highly conserved molecule may also be important for the vascular interaction mechanisms of other pathogens.