ction. Host-targeted insecticides, deer fencing and personal protection may help reduce environmental risk and prevent LD (Fish, 1995).
Early infection is characterized by skin lesions. Next, various organs may be affected. Frequent manifestations are found in the skin, nervous system musculoskeletal system, and the heart. Ocular involvement may occur in early disseminate and chronic stages. Ocular Lyme borreliosis may be the cause of conjunctivitis, keratitis, iridocyclitis, intermediate uveitis, vitretis, retinal vasculitis, chorodiditis, optic neuritis, and cranial nerve palsy (Suttorp-Schulten, Kuiper, Kijlstra, van Dam, & Rothova, 1993).
After Bb is inoculated by the tick into the skin, it goes through the extracellular matrix; this may explain the expansion of the EM rash. Bb binds to extracellular matrix components, which include epithelial cell-derived proteoglycans (heparin, heparan sulfate, and dermatan sulfate), collagen (by interacting with decorin), glycosaminoglycans, and fibronectin. Bb binds to glycosphingolipids on the surface of neural cellular elements and to platelets, red blood cells, and dextran (Sigal, 1997).
Bb escapes the skin, via spirochetemia, and goes to other organs; this multifocal dispersal of Bb by spirochetemia leads to early disseminated LD. It binds cultured glioma and glial cells, Vero, HeLa, and WISH cells; it also binds human plasminogen. A later symptoms of LD, noninflammatory joint disease, may be from circulating cytokines; however, it is believed that arthritis is related to local infection with Bb (Sigal, 1997).
Interaction of spirochete and immune systems is complex in LD. T cells and macrophages are associated with arthritis pathogenesis and immune mechanisms are affected by Bb. In hamsters, a destructive arthritis was induced upon challenge with viable Bb; this suggested that macrophages have a role, possibly by recruiting and activating T cells. Bb induces cha...