Borrelia infectie in de hersenen

[Sproetje]

http://www.neurology.org/content/40/10/1535.short

Borrelia burgdorferi infection of the brain

Characterization of the organism and response to antibiotics and immune sera in the mouse model

Andrew R. Pachner, MD and Andrea Itano, BS

1990

Abstract

To learn more about the neurologic involvement in Lyme disease, we inoculated inbred mice with the causative agent of Lyme disease, Borrelia burgdorferi. We cultured brains and other organs, and measured anti-B burgdorferi antibody titers. We further studied a brain isolate for its plasmid DNA content and its response in vitro to immune sera and antibiotics. One strain of B burgdorferi, N40, was consistently infective for mice, and resulted in chronic infection of the bladder and spleen. SJL mice developed fewer culture-positive organs and had lower antibody titers than Balb/c and C57B1/6 mice. Organism was cultured from the brain early in the course of infection, and this isolate, named N40Br, was further studied in vitro. The plasmid content of N40Br was different from that of the infecting strain, implying either a highly selective process during infection or DNA rearrangement in the organism in vivo. N40Br was very sensitive to antibiotics, but only after prolonged incubation. Immune sera from both mice and humans infected with B burgdorferi were unable to completely kill the organism by complement-mediated cytotoxicity. These data demonstrate that B burgdorferi infects the brain of experimental animals, and is resistant to immune sera in vitro but sensitive to prolonged treatment with antibiotics.

[Sproetje]

Interaction of the Lyme Disease Spirochete Borrelia burgdorferi with Brain Parenchyma Elicits Inflammatory Mediators from Glial Cells as Well as Glial and Neuronal Apoptosis


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570132/

Geeta Ramesh,* Juan T. Borda,† Jason Dufour,‡ Deepak Kaushal,* Ramesh Ramamoorthy,* Andrew A. Lackner,† and Mario T. Philipp*
2008

Abstract


Lyme neuroborreliosis, caused by the spirochete Borrelia burgdorferi, often manifests by causing neurocognitive deficits. As a possible mechanism for Lyme neuroborreliosis, we hypothesized that B. burgdorferi induces the production of inflammatory mediators in the central nervous system with concomitant neuronal and/or glial apoptosis. To test our hypothesis, we constructed an ex vivo model that consisted of freshly collected slices from brain cortex of a rhesus macaque and allowed live B. burgdorferi to penetrate the tissue. Numerous transcripts of genes that regulate inflammation as well as oligodendrocyte and neuronal apoptosis were significantly altered as assessed by DNA microarray analysis. Transcription level increases of 7.43-fold (P = 0.005) for the cytokine tumor necrosis factor-α and 2.31-fold (P = 0.016) for the chemokine interleukin (IL)-8 were also detected by real-time-polymerase chain reaction array analysis. The immune mediators IL-6, IL-8, IL-1β, COX-2, and CXCL13 were visualized in glial cells in situ by immunofluorescence staining and confocal microscopy. Concomitantly, significant proportions of both oligodendrocytes and neurons undergoing apoptosis were present in spirochete-stimulated tissues. IL-6 production by astrocytes in addition to oligodendrocyte apoptosis were also detected, albeit at lower levels, in rhesus macaques that had received in vivo intraparenchymal stereotaxic inoculations of live B. burgdorferi. These results provide proof of concept for our hypothesis that B. burgdorferi produces inflammatory mediators in the central nervous system, accompanied by glial and neuronal apoptosis.


Lyme disease is a tick-borne infection caused by the spirochete Borrelia burgdorferi (sensu lato).1,2 The remarkable organ pleiotropism of this spirochete results in diverse disease manifestations such as acute or chronic arthritis, myocarditis, and neuroborreliosis.3 Lyme neuroborreliosis affects 15 to 25% of patients with erythema migrans, the red skin-rash that in humans signals the point of entry of B. burgdorferi, and may involve both the peripheral and central nervous systems (CNS).

Neuroborreliosis may manifest early, within the first few weeks to months of the appearance of erythema migrans, as a meningitis, often as part of the Garin-Bujadoux-Bannwarth syndrome, or, more seriously, as encephalomyelitis.
..................

[Sproetje]

Adherence of the Lyme Disease Spirochete to Glial Cells and Cells of Glial Origin

Juan Carlos Garcia-Monco, Beatriz Fernandez-Villar and Jorge L. Benach
1989

http://jid.oxfordjournals.org/content/1 ... 7.abstract

Abstract

Lyme disease, a tick-borne spirochetosis caused by Borrelia burgdorferi, produces protean neurologic manifestations, yet its neuropathogenesis is poorly understood. The affinity of the spirochete for cells of primary rat brain cultures and of the C6 glioma cell line was studied. B. burgdorferi adhered to both types of cells in a dose-dependent manner and exhibited an affinity for an extracellular matrix produced by the primary and by glioma cell cultures. Adherence of the spirochetes to the glial components of the primary brain culture could be an early event in the production of neurological injury; its affinity for cells could be the reason for its infrequent isolation from cerebrospinal fluid.

[Sproetje]

The Pathogenesis of Lyme Neuroborreliosis: From Infection to Inflammation

Tobias A Rupprecht,1 Uwe Koedel,1 Volker Fingerle,2 and Hans-Walter Pfister1
2008


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2148032/

Abstract


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, we discuss the mechanisms by which the spirochetal infection leads to the observed neural dysfunction. To conclude, we construct a stringent concept of the pathogenesis of LNB.

[Sproetje]

Persisting atypical and cystic forms of Borrelia burgdorferiand local inflammation in Lyme neuroborreliosis

Judith MiklossyEmail author, Sandor Kasas, Anne D Zurn, Sherman McCall, Sheng Yu and Patrick L McGeer
2008


http://jneuroinflammation.biomedcentral ... -2094-5-40

Conclusion

The results indicate that atypical extra- and intracellular pleomorphic and cystic forms of Borrelia burgdorferi and local neuroinflammation occur in the brain in chronic Lyme neuroborreliosis. The persistence of these more resistant spirochete forms, and their intracellular location in neurons and glial cells, may explain the long latent stage and persistence of Borrelia infection. The results also suggest that Borrelia burgdorferi may induce cellular dysfunction and apoptosis. The detection and recognition of atypical, cystic and granular forms in infected tissues is essential for the diagnosis and the treatment as they can occur in the absence of the typical spiral Borrelia form.

[VerlorengezondheidM]

1995.....

Seronegative chronic relapsing neuroborreliosis.

Abstract
We report an unusual patient with evidence of Borrelia burgdorferi infection who experienced repeated neurologic relapses despite aggressive antibiotic therapy. Each course of therapy was associated with a Jarisch-Herxheimer-like reaction. Although the patient never had detectable free antibodies to B. burgdorferi in serum or spinal fluid, the CSF was positive on multiple occasions for complexed anti-B. burgdorferi antibodies, B. burgdorferi nucleic acids and free antigen.

Bron: NCBI

[Henriëtte]

How Lyme Disease can affect the brain;

What causes Brain Fog?

Another possible explanation for brain fog is in regards to the toxins that emerge constantly from Lyme disease. Lyme typically releases two types of toxin into the body. Exotoxins are the toxins that are continuously released as waste material. Endotoxins are the toxins released when cell walls are damaged or destroyed. These walls are damaged when antibiotics or the immune system starts working.
Lyme has also shown links with the release of ammonia, a substance linked to Alzheimer’s. This exotoxin can disrupt proper brain function, and it is common for people with Lyme to have high levels of ammonia. An inability to detox the system from this substance properly can lead to severe problems with memory loss, and even chronic issues.
Additionally, the endotoxins that Lyme releases when the cell wall is destroyed can accumulate in the brain without a detoxification process. The result can be the destruction of brain tissue or neurons which brings on symptoms like Alzheimer’s. The presence of endotoxins can call upon the reaction of the immune system, which releases cytokines.
Cytokines can exacerbate symptoms within the body and the brain. This is why many professionals believe that it is important to reduce the inflammation that happens in Lyme patients. In order for Lyme patients to heal, they must remove inflammation, and this often begins with adaptations to the diet. Many Lyme disease experts recommend removing dairy, sugars, and gluten from the diet, because these products can all cause inflammatory responses in the body.

http://drjaydavidson.com/lyme-disease-affect-brain/

Henriëtte

[Sproetje]

Brainstem abnormalities and vestibular nerve enhancement in acute Neuroborreliosis

Nadja A Farshad-Amacker,1 Hans Scheffel,1 Thomas Frauenfelder,1 and Hatem Alkadhi1
Zwitserland
2013

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3878100/

Background
Borreliosis is a widely distributed disease. Neuroborreliosis may present with unspecific symptoms and signs and often remains difficult to diagnose in patients with central nervous system symptoms, particularly if the pathognomonic erythema chronica migrans does not develop or is missed. Thus, vigilance is mandatory in cases with atypical presentation of the disease and with potentially severe consequences if not recognized early. We present a patient with neuroborreliosis demonstrating brain stem and vestibular nerve abnormalities on magnetic resonance imaging.

[Henriëtte]

Study: Living Lyme disease bacteria found months after antibiotic treatment;

Rare, but intact B. burgdorferi spirochetes were found in the tissues of both the treated and untreated subjects. In two subjects treated with doxycycline, multiple Lyme bacteria were observed in the brain tissue. Others organs in which the spirochetes were observed included the heart, joints, bladder, skeletal muscle and adjacent to peripheral nerves.

https://www.news-medical.net/news/20171 ... tment.aspx

Henriëtte

[Henriëtte]

The Sneaky Explanation Behind Increased Painful Lyme Disease Symptoms;

The illness can lead to arthritis and carditis, and when the nervous system is involved, called Lyme neuroborreliosis (LNB), it can cause muscle weakness, sensory loss, facial nerve palsy, and limb and neurogenic pain in the back, legs, and feet.

Researchers from the Tulane National Primate Research Center and Louisiana State University Health Sciences Center explored how inflammation levels in the central nervous system, spinal nerves, and dorsal root ganglia (DRG) played a role in symptom intensity.

“These results suggest that inflammation has a causal role in the pathogenesis of acute Lyme neuroborreliosis,” one of the authors Mario T. Philipp, PhD, said in a news release.

we found necrotizing myelitis and degeneration in the spinal cord, neurodegeneration in the dorsal root ganglia, and demyelination in the nerve roots only when lymphocytic inflammatory lesions were also observed in both the central nervous system and peripheral nervous system,

https://www.mdmag.com/medical-news/the- ... e-symptoms

Henriëtte