The African relapsing fever spirochete Borrelia crocidurae forms aggregates
with erythrocytes, resulting in a delayed immune response. Mice were infec
ted with B. crocidurae and monitored during 50 days after infection. Spiroc
hetes were observed extravascularly at day 2 after infection. Two days late
r, inflammatory responses, cell death, and tissue damage were evident. The
pathologic responses in lungs and kidneys were similar, whereas the symptom
s in the brains were delayed, with a less pronounced inflammatory response.
Microemboli were found in the blood vessels, possibly a result of the eryt
hrocyte aggregation. The B. crocidurae invasion emerged more rapidly than h
as been described for Lyme disease-causing Borrelia species. In addition to
erythrocyte resetting, the presence of extravascular B. crocidurae indicat
es a novel route for these bacteria to propagate and cause damage in the ma
mmalian host. The histopathologic findings in this study may explain the cl
inical manifestations of human relapsing fever.