Borrelia burgdorferi adhere to blood vessels in the dura mater and are associated with increased meningeal T cells during murine disseminated borreliosis
Published: May 3, 2018 https://doi.org/10.1371/journal.pone.0196893
Borrelia burgdorferi, the causative agent of Lyme disease, is a vector-borne bacterial infection that is transmitted through the bite of an infected tick. If not treated with antibiotics during the early stages of infection, disseminated infection can spread to the central nervous system (CNS). In non-human primates (NHPs) it has been demonstrated that the leptomeninges are among the tissues colonized by B. burgdorferi spirochetes. Although the NHP model parallels aspects of human borreliosis, a small rodent model would be ideal to study the trafficking of spirochetes and immune cells into the CNS. Here we show that during early and late disseminated infection, B. burgdorferi infects the meninges of intradermally infected mice, and is associated with concurrent increases in meningeal T cells. We found that the dura mater was consistently culture positive for spirochetes in transcardially perfused mice, independent of the strain of B. burgdorferi used. Within the dura mater, spirochetes were preferentially located in vascular regions, but were also present in perivascular, and extravascular regions, as late as 75 days post-infection. At the same end-point, we observed significant increases in the number of CD3+ T cells within the pia and dura mater, as compared to controls. Flow cytometric analysis of leukocytes isolated from the dura mater revealed that CD3+ cell populations were comprised of both CD4 and CD8 T cells. Overall, our data demonstrate that similarly to infection in peripheral tissues, spirochetes adhere to the dura mater during disseminated infection, and are associated with increases in the number of meningeal T cells. Collectively, our results demonstrate that there are aspects of B. burgdorferi meningeal infection that can be modelled in laboratory mice, suggesting that mice may be useful for elucidating mechanisms of meningeal pathogenesis by B. burgdorferi.
It is thue that Borrelia invade the brain, causing Lyme Meningitis or Lyme Encephalitis, associated with cranial pressures and pain. Can be treated with antibiotics able to penetrate the BBB, Minocycline and Tindamax. Also it is very important to treat the cyst forms and Borrelia biofilms. There are at least 3 infective forms of the pathogen Borrelia:
1. Motile Borrelia (live bacteria)
2. Cyst forms (protected bacterial genome) able to generate live spirochètes, later when the conditions are ok.
3. Borrelia biofilms.
Each transformation cycle should be treated with different bactericidal antibiotics, the dosage is very important and the length of the treatment protocol, because Borrelia replication cycle is very slow.
Which explains the memory lapse, brain fog, headaches! It’s hard when you Elisa tests (4) come out negative and yet I had 4 bites, one was a full Bull’s eye. Only had 2 weeks of Doxicycline (ER doctor) and still had persistent symptoms. Went to see family physician and didn’t want to give more antibiotics. Really frustrating!!! Now I’m always in pain!
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