Abstract
Lyme disease affects several major organ systems and leads to chronic illness. The pathogenesis of this disease appears to be centered around the long-term persistence of the organisms in tissues. In Lyme disease, isolations of B. burgdorferi are rare. It is though that few organisms actually invade the host and that host mediators amplify the inflammatory response. Immune and nonimmune phagocytosis leading to bacterial killing occurs in Lyme disease. This organism shows preference for cell surfaces and tissues which may explain the paucity of isolations but also displays characteristic nonspecificity in its adherence to eukaryotic cells. This lack of specificity may explain its capacity to reside and injure vastly different tissues. Autoimmune mechanisms may coincide with spirochetal persistence in the pathogenesis of chronic Lyme disease.
| Original language | English |
|---|---|
| Pages (from-to) | 711-726 |
| Number of pages | 16 |
| Journal | Rheumatic Disease Clinics of North America |
| Volume | 15 |
| Issue number | 4 |
| State | Published - 1989 |
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