Welkom bij het Lymeforum

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15. Persistence of spirochetes within macrophages
Of course mice aren't human, but they are part of the chain of evidence from tick to mouse to tick to human- so we are allowed to apply logic in "Demonstration".
Malawista et al. in J Immunol 1993 Feb 150:909-15 clearly demonstrate the Bb spirochetes living within macrophages by scanning confocal microscopoy at multiple times after infection. "Persistence of spirochetes within macrophages provides a possible pathogenetic mechanism for chronic or recurrent Lyme disease in man".
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9. Bb present from healed site of erythema migrans

Next we have isolation of Bb from biopsy specimens taken from healthy looking skin of patients with Lymeborreliosis (Kuiper J Clin Microbiol 1994 Mar 32 .715-20). Six patients have Bb present from healed site of EM up to 6 months later by culture and PCR but not by silver staining. Where is the Bb? ... could be intracellular.
Likewise in PCR reaction for detection of Bb DNA in skin lesions of early and late Lyme borreliosis von Stedingk in Eur J Clin Microbiol Infec Dis 1995 Jan ; 14 ;1-5 found that over 60% of these skin biopsies had Bb DNA and after antibiotic treatment were negative but staining could not demonstrate Bb. Where were they?

Abstract:

Human infection by Borrelia burgdorferi, the etiological agent for lyme disease, can result in seriwus acute and late term disorders including
neuroborreliosis, a degenartive condition of the peripheral and cetral nerous system.
To examine the mechanisms involved in the cellular pathogenesis of neuroborreliosis, we investigeted the abilitky of B. burgdorferi to attach to and/or invade a panel of human neuroglial and cortical
differential immunoflluorescent staining of external and internal organisms, and gentamicin protection assay demonttrated an intracellular localization
of B. burgdorferi.
A non-infectious strain of B. burgdorferi was attenuated in its ability to associate with these neural cells,
suggesting that a specific borrelial factor related to cellular infectivitty was responsible for the association.
Cytopathic effects were nog oberved following infection of these cell lines with B. burgdorferi, and internalized spirochetes were found to be viable.
Invasion of neural cells by B. burgdorferi provides a putative mechanism for the organism to avoid the host's immune response while potentially causing functional damage to neural cells durfing infection of th CNS

Abstract
To investigate if Borrelia burgdorferi can persist in resident joint cells, an infection model using cell cultures of human synovial cells was established and compared to the interaction of Borrelia burgdorferi and human macrophages. Borrelia burgdorferi were found attached to the cell surface or folded into the cell membrane of synovial cells analysed by transmission electron and confocal laser scanning microscopy. In contrast to macrophages, morphologically intact Borrelia burgdoJferi were found in the cytosol of synovial cells without engulfment by cell membrane folds or phagosomes. Borrelia burgdotferi were isolated from parallel cultures. Treatment with ceftriaxone eradicated extracellular Borrelia burgdorferi, but spirochetes were reisolated after lysis of the synovial cells. Borrelia burgdorferi persisted inside synovial cells for at least 8 weeks. These data suggested that Borrelia burgdorferi might be able to persist within resident joint cells in vivo.

There are a number of factors that are secreted either by B. burgdorferi itself or in response to infection with the spirochete [44,45,46,47,48,49,50–51]. For a number of years, it has been known that B. burgdorferi secretes a hemolysin, although its function is uncertain [44]. More recently, the spirochete has been shown to elaborate porin and adhesin, 2 proteins that allow bacteria to adhere to cells and pierce the cell wall to gain entry