Objectives Assess infection of the central nervous system (CNS) by B. burgdorferi (Bb) in the rhesus monkey. Results Five age-matched male rhesus macaques were needle-inoculated with a neurotropic strain of B. burgdorferi (NT1). One animal was left uninfected, as a control. All animals, except the control, were verified to be infected by recovering Bb, and amplifying Bb DNA, from skin biopsy samples. Infection was monitored longitudinally by determining the titer of anti-P39 antibodies and number of bands detected on Western blots. CNS infection was monitored by determining, cerebral spinal fluid (CSF) pleocytosis, presence of Bb DNA in CSF, (by nested PCR) and production of intrathecal anti-Bb antibodies. CNS disease was monitored by measuring somatosensory evoked potentials (SEP) recorded from both upper and lower extremities immediately following infection, and longitudinally over a period of nine months. The level of anti-P39 antibodies and the number of antigen bands on IgG West ern blots increased until week 10 post-infection (PI), and then remained essentially unchanged until the end of the study (90 weeks PI). This suggest that the animals remained infected throughout the study period. CSF pleocytosis, and presence of B. burgdorferi DNA in the CSF were observed in all animals at different periods within the first 20 weeks PI. Intrathecal anti-Bb antibody ptoduction was also oberved in some animals within the 90 week study period. Two animals showed significant changes which are consistent with abnormalities in the central somatosensory system, one animal by weeks 11 and 35 PI, and the other at week 35 PI. Peripheral nerve function was found to be normal in the nerves that were selected to determine SEP, thus indicating that these changes were based in the central somatosensory pathway. Our study contributes solid and conclusive evidence that infection of the rhesus monkey with B. burgdorferi causes not only infection and disease of the peripheral nervous sy stem, as we have already demonstrated, but also of the CNS. Future directions A thorough survey of brain pathology in these animals is underway. FUNDING CDC Cooperative Agreement (U50/CCU606604-07) and Base grant. PUBLICATIONS Roberts, E. D., Bohm, Jr., R. P., Lowrie, Jr., R. C., Habicht, G., Piesman, J. and Philipp, M. T. 1998. Pathogenesis of Lyme Neuroborreliosis in the Rhesus Monkey the Acute and Chronic Phases of Disease in the Peripheral Nervous System. J. Infect. Dis. 178, 722-732.