Peripheral neuropathy is a recognized but poorly understood manifestat
ion of Lyme disease. We performed serial electrophysiological studies
on 8 rhesus monkeys chronically infected with the JD1 strain of Borrel
ia burgdorferi and compared the results with those of similar studies
on 10 uninfected control monkeys. Four infected and 2 uninfected anima
ls underwent sural nerve biopsy. Five of the infected and 1 of the uni
nfected animals also had postmortem neuropathological examinations. Al
together, 5 of the infected monkeys demonstrated primarily axonal-loss
-variety multifocal neuropathies. Only one nerve lesion exhibited find
ings compatible with demyelination. Pathologically, peripheral nerve s
pecimens showed multifocal axonal degeneration and regeneration and oc
casional perivascular inflammatory cellular infiltrates without vessel
wall necrosis. Free spirochetal structures were not seen, but several
macrophages exhibited positive immunostaining with a highly specific
anti-B. burgdorferi, 7.5-kd lipoprotein monoclonal antibody. In the in
fected animals, serial analysis of serum antibodies to B. burgdorferi
showed increasing numbers of IgG specificities and new IgM specificiti
es, suggesting persistent infection. Thus, peripheral neuropathy in th
e form of a mononeuropathy multiplex develops frequently in rhesus mon
keys chronically infected with B. burgdorferi. The pathogenesis of the
se nerve lesions is not yet known, but our studies suggest an immune-m
ediated process perhaps driven by persistent infection with B. burgdor
feri.