Antibodies to the outer surface proteins (Osps) A, B, and C of the spi
rochete Borrelia burgdorferi can prevent infection in animal models of
Lyme borreliosis. We have previously demonstrated that immune serum f
rom mice infected with B. burgdorferi N40 can also prevent challenge i
nfection and induce disease regression in infected mice. The antigens
targeted by protective and disease-modulating antibodies are presently
unknown, but they do not include Osp A or Osp B. Because Osp C antibo
dies are present in immune mouse serum, we investigated the ability of
hyperimmune serum to recombinant Osp C (N40) to protect mice against
challenge infection with N40 spirochetes. In both active and passive i
mmunization studies, Osp C (N40) antiserum failed to protect mice from
challenge infection with cultured organisms. Mice actively immunized
with recombinant Osp C (N40) were susceptible to tick-borne challenge
infection, and nymphal ticks remained infected after feeding on Osp C-
hyperimmunized mice. In contrast, similar immunization studies perform
ed with Osp C (PKo) antiserum prevented challenge infection of mice wi
th a clone of PKo spirochetes pathogenic for mice. Both Osp C (N40) an
d Osp C (PKo) antisera showed minimal in vitro borreliacidal activity,
and immunofluorescence studies localized Osp C beneath the outer memb
rane of both N40 and PKo spirochetes. We conclude that Osp C antibody-
mediated immunity is strain specific and propose that differences in O
sp C surface expression by spirochetes in vivo may account for strain-
specific immunity.