Lyme Disease - Epidemiology and Pathophysiology

Lyme disease is a zoonosis caused by the spirochete Borrelia burgdorferi and its genospecies. Its distribution includes Europe and some parts of North America. The dominant vector in Europe is the tick Ixodes ricinus. Its three developmental stages (larvae, nymph, adult) take blood meals from small rodents, birds, and deer, some of which may also host B. burgdorferi. This is how the majority of the ticks become infected. Transmission of the pathogen to a new host occurs via tick saliva at the next blood meal, which induces phenotypical modifications of the spirochete that facilitate migration from the tick intestine to the salivary gland and survival in the vertebrate host. Both, tick saliva and the remodeled surface proteins of the bacteria, provide protection from the host's immune system. Dissemination occurs predominantly via the hematogenous route, but motility of the spirochete facilitates tissue migration. The species-dependent tropism for skin, joints and neuronal structures appears to be mediated by specific interactions between host and pathogen proteins. While extrapolated total cases of Lyme disease in Switzerland have remained stable over the past years, areas where infected ticks can be found have expanded. Milder winters and higher temperatures may explain this observation. In addition to measures helping to avoid tick bites, vaccines may contribute to protect against Lyme disease in the future. A promising, multivalent, protein-based vaccine appears to provide protection from several subspecies of B. burgdorferi.