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Central and peripheral nervous system infection, immunity, and inflammation in the nonhuman primate model of lyme borreliosis
Author(s) -
Pachner Andrew R.,
Cadavid Diego,
Shu Gale,
Dail Donna,
Pachner Sarah,
Hodzic Emir,
Barthold Stephen W.
Publication year - 2001
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.1287
Subject(s) - borrelia burgdorferi , lyme neuroborreliosis , neuroborreliosis , immunology , lyme disease , inflammation , antibody , cerebrospinal fluid , central nervous system , biology , spirochaetaceae , medicine , pathology , endocrinology
The relationship between chronic infection, antispirochetal immunity, and inflammation is unknown in Lyme neuroborreliosis. In the nonhuman primate (NHP) model of Lyme neuroborreliosis, we measured spirochetal density in the nervous system and other tissues by polymerase chain reaction and correlated these values to anti‐ B. burgdorferi antibody in the serum and cerebrospinal fluid, and to inflammation in tissues. Despite substantial presence of B. burgdorferi , the causative agent of Lyme borreliosis, in the central nervous system, only minor inflammation was present there, though skeletal and cardiac muscle, which contained similar levels of spirochete, were highly inflamed. Anti‐ B. burgdorferi antibody was present in the cerebrospinal fluid but was not selectively concentrated. All infected animals developed anti‐ B. burgdorferi antibody in the serum, but increased amplitude of antibody was not predictive of higher levels of infection. These data demonstrate that Lyme neuroborreliosis is a persistent infection, that spirochetal presence is a necessary but not sufficient condition for inflammation, and that antibody measured in serum may not predict the severity of infection.