Na de tekenbeet : man valt zijn vrouw aan

[lulu]

We hebben het over een ziektebeeld waarbij de pathofysiologie nog niet bekend is, het heeft ook geen zin om daar verhalen bij te verzinnen, over stofjes die dit, bacteriën die dat. We weten dat immers niet.

Wat we wel weten is dat er een invaliderend ziektebeeld ontstaat die neurologische, cognitieve en stemmingsproblematiek geeft. Het zou al heel wat zijn als dit systematisch in kaart werd gebracht, het ziektebeeld an sich.

De meest waarschijnlijke verklaring is dat er, net als bij chronische Q-koorts, ME, MS, een chronische low-graded herseninflammatie ontstaat met alle gevolgen op het autonoom zenuwstelsel (hart, bloeddruk, POTS, OI), stemmingsregulatie, geheugen, concentratie. Inflammatie is een lichaamseigen reactie, dit kan maar hoeft niet op te treden door een agens. Bij ons ziektebeeld waarschijnlijk tgv een falend immuunsysteem.

Zie ook het artikel van Nakatomi:
"Neuroinflammation is present in widespread brain areas in CFS/ME patients and was associated with the severity of neuropsychologic symptoms. Evaluation of neuroinflammation in CFS/ME patients may be essential for understanding the core pathophysiology and for developing objective diagnostic criteria and effective medical treatments."

[Foetsie]

Maar het is wel aangetoond dat Bb geen toxines produceert.

Ook dat is toch nog iets genuanceerder:

(Lees vooral de eerste alinea):

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1082833/


Verder; Stel het zou in 1 onderzoek dat gepubliceerd wordt aangetoond zijn (wel/geen produceren van toxines v.d. borrelia burgdorferi), dan nog zouden er meerdere onderzoeken moeten volgen.

[Foetsie]

De toxines ontstaan bij deze bacteriën na cellysis.

Bedoel je daarmee het afsterven van de cellen van de Bb of van de mens?


Op welke artikelen baseer je dit?

[Damrak]

While I know what I posted before - that there is no LPS in Borrelia and therefore, by definition, no endotoxin or no toxins involved in Bb infection - there are a few things to keep in mind:

1) There has been research on the kynurenine-pathway mediated excitotoxicity which occurs in Lyme neuroborreliosis and to lesser degree, encephalopathy - that is, the immune system responds to the infection and an excitotoxin is produced in the brain (quinolinic acid) which increases the accumulation of glutamate at the synapses while calcium overloads neurons. See: http://campother.blogspot.com/2012/04/f ... might.html

2) There has been research which suggests that highly immunogenic outer surface proteins have an endotoxin-like profile - but only if the lipid moiety is included. OspA peptides on their own are not that immunogenic.

3) All this said, one should note a recent study which I linked to on my blog recently, one conducted at the NIAID:

Project: A COMMON DENOMINATOR OF PATHOGENESIS; A RARE OPPORTUNITY FOR NOVEL THERAPEUTIC DE(VELOPMENT)
Institution: UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN
PI: Mitchell, Douglas

Description (by applicant):

Abstract: The 20th century witnessed several major advances in medicine. Perhaps most important were the discovery of antibiotics for bacterial infections and effective vaccines for several major viruses. Unfortunately, the creation of effective vaccines for bacteria has lagged behind analogous anti-viral strategies. Compounded with the rise in antibiotic resistance and a lack of interest from the pharmaceutical industry in pursuing novel antibiotics, we risk losing the fight against bacterial pathogens.

Described herein is an unconventional strategy to exploit bacterial toxins as both novel targets for antibacterial agents and antigens for vaccine development. To intelligently address the increasing threat posed by bacterial pathogens, more effort is needed to uncover the molecular underpinnings of virulence. Our group specializes in the use of bioinformatics, in vitro reconstitution, and genetic manipulation to identify and characterize gene clusters that are responsible for the biosynthesis of virulence-promoting cytolysins. The best-known toxin in this family is the highly modified peptide, streptolysin S (SLS, produced by Streptococcus pyogenes).

SLS production is required for the infective process, but not essential life processes. Our work has uncovered SLS-like toxins are synthesized by at least three other notorious human pathogens, including Staphylococcus aureus, Listeria monocytogenes, and Clostridium botulinum. We aim to study the potential role of the SLS-like toxin in an additional organism, Borrelia burgdorferi (Bb), which causes Lyme disease.

Although widely known, the Bb molecular mechanism of pathogenesis is inadequately defined. If the SLS-like toxin was indeed employed during Bb infections, this would represent the first demonstration of toxin utilization in this family of organisms and would prompt a major revision of borrelioses.

Because bacteria typically employ disparate pathogenic mechanisms, the conserved, SLS-like pathway provides a rare opportunity to develop more broadly applicable, yet targeted countermeasures. From our perspective, new antimicrobial strategies should directly target the pathogenic mechanism, rather than DNA replication, protein synthesis, or the cell wall. This approach holds enormous potential, as these drugs will theoretically be resistant to resistance.

This project will identify inhibitors of SLS toxin biosynthesis for the specific purpose of developing novel antibacterials. Moreover, SLS is non-immunogenic, rendering it an unfeasible candidate for vaccine development.

We have succeeded in generating attenuated variants with the anticipation that these can be used for raising toxin-neutralizing antibodies. The notion of immunizing against a bacterial toxin represents a potentially general strategy for future vaccine development.

With this proposal, we aim to not only fundamentally shift the accepted view of Bb pathogenesis, but also to challenge the paradigm that antibiotics must kill bacteria and non-immunogenic toxins are intractable vaccine candidates. These seemingly unrelated goals are actually quite intertwined. Our approach rests on the philosophy that a more complete understanding of toxin biosynthetic pathways and chemical structure can be rationally exploited to design novel therapeutics.

Public Health Relevance: Bacterial pathogens employ numerous mechanisms to evade the human immune system. We have discovered a novel strategy within the organism that causes Lyme Disease, who's pathogenesis remains largely enigmatic. A greater understanding of these processes will lay the foundation for developing the next generation of antimicrobial drugs.

Link: http://projectreporter.nih.gov/project_ ... e=12284856

[Foetsie]

Damrak,

Ik kan je onderste link niet openen, omdat ie is gekopieerd en/of er verschijnt geen text (txt robot)


Dit is i.i.g. de eerste link:


http://campother.blogspot.nl/2012/04/fa ... might.html

Dank voor je artikel.

[Damrak]

http://projectreporter.nih.gov/project_ ... e=12284856

Excuus!