ABSTRACT
Most of the clinical manifestations of Lyme disease are due to the local presence
of the causative agent, Borrelia burgdorferi , in the affected tissues. However, the precise means of tissue damage are not well
understood and there is no proof that the organism, live or dead, is always present. An understanding of the complex interaction between the organism, the immune
response elicited by the organism, and the host can explain manifestations of the
disease and persistence of symptoms and signs after the antibiotic-induced death of
the organism. It is possible that dead spirochetes, or fragments thereof may persist
and act as a focus of ongoing inflammation. Different immunogenetic types may predispose
to different immunologic responses, with distinct clinical outcomes. Vascular changes
induced by the infection, either by local infection or the effects of cytokines on
the vessel wall, may underlie tissue pathology. Finally, the immune response to B. burgdorferi may elicit the production of antibodies capable of recognizing and damaging or modifying
normal host tissues. Only by establishing the mechanisms causing tissue damage in
Lyme disease can rational therapeutic strategies be developed. Only by understanding
these mechanisms can physicians and patients interpret clinical responses to therapy
and accurately appreciate the clinical prognosis.
Keywords
Immunopathogenesis - molecular mimicry - auto-immunity - antigen-induced arthritis
model - vasculitis - axonopathy - flagellin
