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Lyme disease is a multisystemic disorder caused by infection with Borrelia burgdorferi sensu lato which is carried by ticks of the Ixodes ricinus complex. The agent was discovered in 1982 in North America and the
disease is recognized as an emerging infectious diseases in North America and Europe. Japanese Borrelia isolates were characterized by genetic and immunologic analysis. Isolates from Ixodes ovatus were found to be unique by DNA/DNA hybridization analysis, restriction fragment length polymorphism analyses of the flagellin gene and the 16S rRNA genes, and were described as new species, Borrelia japonica. Isolates from Ixodes persulcatus were determined as Borrelia garinii and Borrelia afzelii. However, B. garinii found in Japan was different from those from Europe in immunologic and genetic characteristics of outer surface protein A, but B. afzelii isolates from Japan and Europe were identical. An experimental model of arthritis related to
Lyme disease using outbred ddY mice was established. Whole cell vaccine prepared from North American and European isolates could not elicit protective immunity against infection of Japanese isolates. This implies that vaccine development using Japanese isolates is necessary. Borrelia bound specifically to galactosylceramide (GalCer), glucosylceramide and lactosylceramide which are present in various types of cells as binding receptor, but not to other glycosphingolipids. Furthermore, the infectivity of Borrelia may be associated with the binding to glycosphingolipids on the cell surface and a 67 kilodalton protein of
Lyme disease Borrelia may be involved in binding of Borrelia to GalCer.