Although there are several animal models of Lyme disease, only the rhe
sus monkey model exhibits all of the key manifestations of the disease
. After infection with Borrelia burgdorferi, rhesus monkeys develop si
gns of early localized, early disseminated, and chronic Lyme disease.
Specific features include erythema migrans, uveitis, myocarditis, arth
ritis, and disease of the peripheral and central nervous system. One o
f the unique features of the rhesus monkey model is the development of
Lyme neuroborreliosis. Peripheral nervous system (PNS) involvement is
usually in the form of a mononeuropathy multiplex with primarily axon
al-loss features. Evidence of central nervous system (CNS) disease has
included CSF pleocytosis, meningeal inflammation, spinal cord lesions
, and polymerase chain reaction (PCR) data consistent with chronic CNS
infection. The pathogenesis of Lyme neuroborreliosis is not well unde
rstood, but it is likely to involve complex interactions between B. bu
rgdorferi and host immune mechanisms.