In their study, the research team took aim at the larval form of the blacklegged tick, the crucial stage during which a tick becomes infected with B. burgdorferi. Normally, uninfected tick larvae pick up the bacterium the first summer of their two-year life cycle while taking their first blood meal from infected small animals, such as the white-footed mouse. The white-footed mouse is considered a key animal reservoir for Lyme disease. One year later, after the larva develops into a nymph, it feeds on a second animal host, possibly a human, infecting that host. Roughly 90 percent of human infections are contracted from nymphal ticks.
The researchers' goal was to reduce the level of B. burgdorferi infection in nymphal ticks. By vaccinating a large sample of white-footed mice, the researchers hypothesized, fewer tick larvae would become infected the first summer and, in turn, fewer nymphs would be capable of transmitting the disease to humans the following summer.
Throughout the summers of 1998 and 2001, researchers trapped and vaccinated a total of more than 900 mice in 12 different forested sites in Connecticut--six unique sites each summer. In half of the sites, mice received injections of active vaccine; in the other six sites, mice received a placebo.
The vaccine contained a recombinant protein--called OspA--normally found on the outer surface of B. burgdorferi in ticks but not in mice. The vaccine is based on one previously used in humans and currently used in dogs. When an infected nymph feeds on an immunized mouse, the animal's antibodies kill the bacterium inside the nymph, preventing the ny
Contact: Jennifer Wenger
NIH/National Institute of Allergy and Infectious Diseases