Borrelia burgdorferi strains (six isolates from North America and 28 isolates from Europe) were analyzed by physicochemical and immunological methods. By SDS-PAGE, all Borrelia burgdorferi strains tested had two major proteins with constant molecular weights of 60 and 41 kDa and one, two, or three variable low molecular weight proteins (OspA = 30-32 kDa, OspB = 34-36 kDa, pC = 21-22 kDa). All combinations--except OspB alone or OspB/pC--were observed. Borrelia burgdorferi strains were different from relapsing fever borreliae by strong reactivity with OspA- and/or pC-specific polyclonal antibodies, whereas relapsing fever borreliae were only weakly reactive. Among 25 Borrelia burgdorferi isolates, seven different serotypes of Borrelia burgdorferi were defined according to their reactivity in the Western blot with three monoclonal OspA-specific antibodies (H5332, H3TS, and LA5), four OspA- or OspB-specific polyclonal antibodies, and 12 polyclonal antibodies against whole borreliae. Antigenic differences between European CSF and skin isolates were observed, all skin isolates (n = 11) belonging to serotype 2 in contrast to only two out of seven CSF isolates. CSF isolates were antigenically heterogenous (serotypes 1, 2, 3, 4, and 5). Serotypes 6 and 7 were represented by two tick isolates, and the other European tick isolates are not yet fully characterized. Antigenic differences between European and North American strains may play a role in differences in the clinical picture of Lyme borreliosis.

No abstract

No abstract

Central nervous system infection with Borrelia burgdorferi, the causative agent of Lyme disease in the USA, manifests itself most frequently in Europe as lymphocytic meningoradiculitis (Bannwarth's syndrome). We examined 12 patients with lymphocytic meningoradiculitis with cerebrospinal fluid (CSF) antibodies against B. burgdorferi to establish whether these antibodies were produced intrathecally or were serum derived. By comparison of titers of antibody to B. burgdorferi with total IgG and antibodies against tetanus toxoid in CSF and serum, we demonstrated intrathecal production of antibodies to B. burgdorferi in 11 patients. Reactions of IgG antibodies in CSF with a panel of borrelial proteins (molecular weights, 22k, 23k, 39k, 41k, 42k, 48k, 60k, 66k, and 75k) were stronger than those of the serum antibodies; patterns of reactivity varied considerably between patients. However, CSF reactions (in comparison to serum reactions) to the 41k protein were stronger in all patients. Examination of CSF for intrathecal production of antibodies to B. burgdorferi is helpful in diagnosing neurological manifestations caused by B. burgdorferi infections.

An indirect immunofluorescence technique for the determination of antibodies against ixodid tick spirochetes is described. Differences in the reactivity between Ixodes ricinus spirochete and Ixodes dammini spirochete antigens were not observed. Cross-reacting antibodies against Treponema pallidum and Treponema phagedenis can be eliminated by quantitative absorption with T. phagedenis. Cross-reactions with leptospira were not observed by immunofluorescence. In the IgM test, false negative reactions caused by high-titered specific IgG antibodies or false positive reactions caused by rheumatoid factor occur. This can be avoided by testing the IgM fraction (19S-IgM-test) or using sera previously treated with anti-IgG serum. Significantly elevated antibody titers against ixodid tick spirochetes were observed in 45% of 44 cases with erythema migrans disease, in 72% of 29 cases of lymphocytic meningoradiculitis, in all of nine patients with acrodermatitis chronica atrophicans and in all of four investigated patients with lymphocytoma (lymphadenosis benigna cutis).