Lyme Disease

Borrelia burgdorferi is a highly motile spirochete with unique pathogenic mechanisms that allow it to evade immune surveillance and establish persistent infection across multiple organ systems. After inoculation from the Ixodes tick salivary glands (requiring 36-48 hours of attachment), the spirochete expresses outer surface protein C (OspC), which facilitates survival in the mammalian host. As the organism disseminates, it switches to expressing VlsE (variable major protein-like sequence, expressed), a surface lipoprotein that undergoes extensive antigenic variation through segmental gene conversion, allowing immune evasion similar to the mechanism used by Trypanosoma species. B. burgdorferi binds to host extracellular matrix proteins (decorin on collagen fibers, fibronectin, glycosaminoglycans) via dedicated adhesins, which explains its tropism for collagen-rich tissues including skin, joints, heart, and meninges. The organism does not produce classical virulence factors (toxins, proteases); rather, tissue damage is primarily immune-mediated. In Lyme arthritis, the spirochete triggers a TH1-dominant inflammatory response with TNF-alpha, IFN-gamma, and matrix metalloproteinase release that damages synovial tissue. In approximately 10% of Lyme arthritis cases, the arthritis persists after adequate antibiotic treatment (antibiotic-refractory Lyme arthritis), likely due to autoimmune mechanisms...