In the January 15 issue of the Journal of Clinical Investigation researchers from Yale University demonstrate that an outer surface protein, OspC, of the organism Borrelia burgdorferi, which causes Lyme disease, is critical for the organism's ability to invade the tick salivary gland and therefore be transmitted from ticks to humans.
Lyme disease was first named in 1977, when arthritis was observed in a cluster of children in Lyme, Connecticut. The bacterium Borrelia burgdorferi is transmitted to humans by the bite of infected deer ticks and in 2002 caused more than 23,000 infections in the United States, mostly localized to California and states in the northeastern, mid-atlantic, and upper north-central regions. Symptoms include a characteristic "bulls-eye" rash at the bite site, fever, malaise, and muscle and joint aches.
When a tick harboring the bacterium engorges, initiating transmission to a new host, B. burgdorferi decreases the expression of the outer surface protein OspA that allows the bacterium to adhere to the tick gut and instead begins expressing an alternative outer surface protein, OspC. In order to determine the function of OspC, Erol Fikrig and colleagues generated a strain of the B. burgdorferi bacterium that was deficient in OspC. These bacteria were able to survive and multiply in feeding ticks; however, they were unable to invade tick salivary glands. The results agreed with their findings that OspC binds to tick salivary gland extracts and that antibody inhibition of OspC inhibits the ability of B. burgdorferi to invade tick salivary glands, and therefore inhibits transmission to a new mammalian host. These insights into pathogen transmission might offer new approaches to reducing the incidence of Lyme disease.