EARLY AND SPECIFIC ANTIBODY-RESPONSE TO OSPA IN LYME-DISEASE

Borrelia burgdorferi (Bb), the cause of Lyme disease, has appeared not to evoke a detectable specific antibody response in humans until long after infection. This delayed response has been a biologic puzzle and has hampered early diagnosis. Antibody to the abundant organism-speci fic outer surface proteins, such as the 31-kD OspA, has rarely been de tected less than 6 mo after infection. Antibody to a less organism-spe cific 41-kD flagellin protein, sharing common determinants with other bacteria and thus limiting its diagnostic potential, mag appear after 4 to 6 wks. To investigate our hypothesis that specific antibody to Os pA may actually be formed early but remain at low levels or bound in i mmune complexes, we analyzed serum samples from patients with concurre nt erythema migrans (EM). This is the earliest sign of Lyme disease an d occurs in 60-70% of patients, generally 4-14 d after infection. We u sed less conventional but more sensitive methods: biotin-avidin Wester n blots and immune complex dissociation techniques. Antibody specifici ty was confirmed with recombinant OspA. Specific complexed antibody to whole Bb and recombinant OspA was detected in 10 of 11 of the EM pati ents compared to 0 of 20 endemic area controls. IgM was the predominan t isotype to OspA in these EM patients. Free IgM to OspA was found in half the EM cases. IgM to OspA was also detected in 10 of 10 European patients with EM who also had reactive T cells to recombinant OspA. In conclusion a specific antibody response to OspA occurs early in Lyme disease, This is likely to have diagnostic implications.