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Originally posted by Areneli:
They are little containers with toxin and they leak it to the surrounding tissue all the time.

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Abstracts???

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Originally posted by Areneli:
Trust me, that is how things are.

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Thats me doubting Thomas.

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Originally posted by Areneli:
Lifewithlyme, it depends where and how many there are.

If you have them in your brain, than slowly released toxin will affect some parts of your brain and will cause symptoms such as inability to focus, some weird pains or fatigue. The sympotoms will depend on cyst location.

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Interaction of Borrelia spirochetes with human mononuclear leukocytes causes production of leukocytic pyrogen and thromboplastin.

Butler T, Spagnuolo PJ, Goldsmith GH, Aikawa M.

Relapsing fever caused by Borrelia spirochetes is characterized by episodes of spirochetemia, fever, and DIC. We examined the ability of Borrelia hermsii to induce production of leukocytic pyrogen and thromboplastin from human blood leukocytes in vitro. Organisms were found devoid of endotoxin by the Limulus assay. Human peripheral blood leukocytes were separated into MNC and PMN fractions and were incubated with two to five spirochetes per cell in 10% human serum. Supernatant fluids from MNC-spirochete mixtures produced mean increases in the temperature of rabbits of 0.80 degree to 1.35 degrees C, which were significantly higher than those caused by supernatant fluids of MNC or spirochetes alone (p less than 0.05). MNC-spirochete mixtures possessed seven to 15 times the thromboplastic activity of MNC suspensions alone, assayed with a modified one-stage prothrombin time. Supernatant fluids of PMNs and spirochetes, on the other hand, did not contain leukocytic pyrogen, and PMN suspensions did not produce thromboplastin. Cycloheximide (10 micrograms/ml), and inhibitor of protein synthesis, completely suppressed both pyrogen and thromboplastin production. Although intracellular spirochetes were observed within phagosomes of blood monocytes by electron microscopy, the production of leukocytic pyrogen and thromboplastin was not significantly altered by serum opsonins or by the inhibitors of phagocytosis cytochalasin B (5 micrograms/ml) or phenylbutazone (2 mg/ml). These results showed that Borrelia spirochetes stimulated human MNCs to produce increased amounts of leukocytic pyrogen and thromboplastin and that this stimulation required de novo synthesis of protein, was not mediated by endotoxin, and was not prevented by omitting opsonic proteins or by inhibiting phagocytosis.

Thats for spirochetes

It is important to understand the nature of the Bb organism. Bb can change its shape from a spiral to a filament, cyst, granule, hooked rod or elbow. These variants are called L-forms, a name given by the Lister Institute where they were first studied. These L-forms are also called cell-wall deficient (CWD) bacteria taking the non-spiral shape when they have lost much of the cell wall. In this form they do not produce an antibody response, as they have no cell wall for the individual's immune system to respond to. Classic L-forms are active metabolism centers for the production of CWD pleomorphic organisms (Bb). In this form they are able to hide within most tissues in the body, thus protecting them from any host response adverse to their well-being. CWD organisms can revert to typical morphology and may revert into adult forms of other genera, depending on the milieu.

Not cyst form its in a cyst form because its either reproducing or hiding. NO cell wall.

Toxins produced as far as I have found from dead pieces of spirochetes.

Thats it bubba

Learn something new everyday huh

Thanks for posting it!

If we can culture the cysts then we should be able to find the toxins inside, but we haven't. Also by most accounts the cycts appear to be metabolically limited. It seems doubtful they could become great factories of toxins,but I am open to that thought.

I just don't think we can say based on our current evidence and methods that Bb is producing any great quantities of toxin and that all herxheimer reactions are caused by toxins.

The work done on Relapsing Fever Borrelia (Thanks Tree) strongly suggests that it is our own body that produces substances that make us feel ill.

To me that is a very very elegant and admirable piece of evolution and adaptation by Borrelia bacteria that to evade the immune system as they change surface antigens and as they replicate, and use receptors on themselves and the host to penetrate cells and transit the body. (See Patricia Rosa RMLs)

Why make toxins to hurt the host at all? From a survival standpoint we don't have a good answer, but if it is the host who is trying to rid the infection and it is the host that makes toxins that makes us ill as we fight the infection: then it all makes much more sense (at least to me)

Rather than carry around complicated enzyme systems and genes and use large amounts of energy to make toxins, instead Bb appears to trick the host into doing all of their work at a minimal cost of energy and nutrients.

I think there are two basic theories and belief systems on this topic.

1) There are those who believe that Borrelia burgdorferi is producing endotoxins and that these can make us feel ill and make us feel even more ill when we kill and release more toxins by killing Bb during antibiotic therapy.

OR

2) Borrelia is not producing any significant toxins and that the host is producing immune products, and inflammatory by products, and that Bb can induce through receptors and antigens cascade reactions that stimulate host enzyme systems including: Fibrinogen pathway, prostaglandin pathways, compliment pathway, plasminogen activation pathway, thromboplasmin, urokinase activation, and metallo matrix protein production of various MMPs and more. Lyme patients experience a herxheimer reaction form antibiotics not because of toxins but rather becuase a bolus of internal bacterial antigen are released and the immune system responds with cytokines, and the particles engulfed by phagocytes steps up immune activation.

It is the Immune Induction Pathway (IIP) that I think there is more proof for and what I ascribe to. But it is also my belief that it is live active infection that is the engine of this immune response and not some lingering autoimmune phenomena.

The reason this is important is because therapies that minimize patient morbidity can may depend on understanding why we are still sick after treatment.