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The Pathogenesis of Lyme Neuroborreliosis - from Infection to Inflammation - Source: Molecular Medicine, Dec 19, 2007

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By Hans-Walter Pfister, MD, et al. • • January 15, 2008

[Note: The full text of this article may be accessed free at PubMed Central. It includes illustrative figures and links to more than 100 footnoted references.]

This review describes the current knowledge of the pathogenesis of acute Lyme neuroborreliosis (LNB), from invasion to inflammation of the central nervous system.

  • Borrelia burgdorferi (B.b.) enters the host through a tick bite on the skin and may disseminate from there to secondary organs, including the central nervous system.
  • To achieve this, B. b. first has to evade the hostile immune system.
  • In a second step, the borrelia have to reach the central nervous system and cross the blood-brain barrier.
  • Once in the cerebrospinal fluid (CSF), the spirochetes elicit an inflammatory response.
  • We describe current knowledge about the infiltration of leukocytes into the CSF in LNB.

    In the final section, the mechanisms by which the spirochetal infection leads to the observed neural dysfunction will be discussed.

    In conclusion, this review will construct a stringent concept of the pathogenesis of LNB.

    Source: Molecular Medicine. 2007 Dec 19. PMID: 18097481, by Rupprecht TA, Koedel U, Fingerle V, Pfister HW. Departments of Neurology and Microbiology, Ludwig-Maximilians University, Munich, Germany. [E-mail:]

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