Pathogenesis of Lyme Neuroborreliosis in the Rhesus Monkey: The Early Disseminated and Chronic Phases of Disease in the Peripheral Nervous System

• Published in: The Journal of infectious diseases 1998-09, Vol.178 (3), p.722-732
• Main Authors: Roberts, E. Donald, Bohm, Rudolf P., Lowrie, Robert C., Habicht, Gail, Katona, Laura, Piesman, Joseph, Philipp, Mario T.
• Format: Article
• Language: English
• Subjects: Animals; Bacterial diseases; Biological and medical sciences; Borrelia burgdorferi; Borrelia burgdorferi Group - genetics; Borrelia burgdorferi Group - immunology; Disease Models, Animal; Experimental bacterial diseases and models; Infections; Infectious diseases; Lesions; Lyme disease; Lyme Disease - etiology; Lyme Disease - immunology; Lyme Disease - microbiology; Lyme Disease - pathology; Lyme neuroborreliosis; Macaca mulatta; Macrophages; Major Articles; Male; Medical sciences; Monoclonal antibodies; Nerves; Peripheral Nervous System - microbiology; Peripheral Nervous System - pathology; Schwann cells; T lymphocytes; Tissue samples
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/515357

The histopathologic and immunohistochemical features of early and late neuroborreliosis of the peripheral nervous system were investigated in rhesus macaques infected with the JD1 strain of Borrelia burgdorferi. Infection was proven by culture or polymerase chain reaction analysis of skin biopsies and indirectly by Western blot analysis. Three months after infection, neuritis involving multiple nerves was the most consistent neurologic manifestation. Both macrophages and B lymphocytes but not T lymphocytes were present in the cellular infiltrates. Axonal structures surrounding infiltrates had changes consisting of demyelination and axonal phagocytosis. Some of the Schwann cells in lesions stained with anti-nitrotyrosine and anti-tumor necrosis factor-α antibodies. B. burgdorferi, or antigens thereof, were visualized immunohistochemically within macrophages. Forty-six months after infection, the most common changes were regenerative, whereas neuritis was infrequent. Aberrant axonal regeneration, irregularly sized myelinated fibers, and fibrosis were frequently observed. Possible mechanisms to explain the appearance and subsidence of Lyme neuritis are discussed.