The Toll of a TLR1 polymorphism in Lyme disease: A tale of mice and men

Abstract

Lyme disease is the most commonly reported vector-borne infection in North America, with 30,000 confirmed and probable cases occurring annually in the U.S. The cause is the spirochetal bacterium Borrelia burgdorferi and the most common clinical manifestation is a cutaneous reaction to infection, called erythema migrans (EM), at the site of the tick bite. In untreated patients, the EM lesion usually resolves in a matter of weeks; however, more than 50% of such patients will go on to develop evidence of extracutaneous infection, such as meningitis, myocarditis, or, most commonly, arthritis (1). An important breakthrough in understanding why these extracutaneous manifestations might occur was the discovery of spirochetemia in at least 40% of patients with EM, providing a plausible mechanism for dissemination of bacteria to distant sites. With this knowledge, it also became apparent that genetically distinct strains of B burgdorferi exist, and that certain subtypes are significantly more likely to be associated with spirochetemia than others. However, the biologic factors responsible for such differences in pathogenicity remain undetermined.