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Neurologic Disease Associated with Mycoplasma pneumoniae Pneumonitis: Demonstration of Viable Mycoplasma pneumoniae in Cerebrospinal Fluid and Blood by Radioisotopic and Immunofluorescent Tissue Culture Techniques

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Presented in part at the Nineteenth Interscience Conference on Antimicrobial Agents and Chemotherapy, 4 October 1979, in Boston, Massachusetts.

▸Requests for reprints should be addressed to Arnold S. Bayer, M.D.; Division of Infectious Disease, Box 15, Harbor-UCLA Medical Center, 1000 West Carson Street; Torrance, CA 90509.

Los Angeles and La Jolla, California

© 1980 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1981;94(1):15-20. doi:10.7326/0003-4819-94-1-15
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Several neurologic syndromes (including Guillain-Barré) complicated Mycoplasma pneumoniae pneumonitis in a young man. At onset of neurologic disease, buffy coat and cerebrospinal fluid cultures on inert media were negative for M. pneumoniae. However, metabolically active mycoplasma were identified in both body fluids by enhanced uptake of 14C-uracil versus 3H-uridine, with marked reduction in normal uridine-to-uracil uptake ratios (> 1000:1) in tissue culture. Uridine-to-uracil ratios were 8.5:1 and 15:1 for buffy coat and cerebrospinal fluid, respectively. Indirect flourescent antibody (FA) studies confirmed the species as M. pneumoniae. In convalescence, uridine-to-uracil ratios and FA studies of buffy coat normalized, indicating clearance of M. pneumoniae from blood. Cell lines inoculated with "convalescent" cerebrospinal fluid showed slightly increased uracil uptake, slightly decreased uptake ratios, and persistent FA staining of approximately 5% of cells, indicating incomplete clearance of M. pneumoniae. Immune complexes were undetectable in either buffy coat or spinal fluid. This indicates that certain M. pneumoniae-associated neurologic disorders may be related to direct neural infection and not immunologically mediated as has been suggested.


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