It is possible to create cell wall deficient bacteria in the lab using simple antibiotics. When this happens, the surface tension of the cell makes the cell go into a shperical shape, but there is no wall. At this point they are very fragile and any disturbance in pressure causes them to rupture.

Is it possible that Bb also does this but is a bit stronger structurally so that somewhat more pressure is needed to rupture them. Maybe this is how HBOT works. It may not be the oxygen that kills them, it might be the relatively rapid change in pressure that causes the capsule to rupture.

This would/could happen if the internal cell pressure increases to a equalibirum value at the higher pressure. Once the pressure is lowered (ie return to sea level), the capsule would be presurized and could then be forced to rupture.

if this was the case, I would guess that HBOT would be most effective while on an abx that would tend to destroy the outer wall.

When the cyst wall is destructed the survival of any B.b inside would depend on what stage of development the egg or spiral form is in & what other abx are being used. etc.

Then there are the blebs, which I am growing more suspicious of as to their true utility.

Since the tests only look for the motile form and remants of itm the question is how many of these other forms are floating around. There MUST be lots of them and they MUST be able to convert to motile form.

It does not make any sense at all that the motile form density is so low (some quote 1 organism per cc) while the tick can feed off of a fraction of a cc of blood and have an 85% chance of gaining the infection. It just does not make any sense.. Something is missing in the picture.

There is a similar problem with syphilis. That disease creates Guma's, bascially large ulcerated areas of infection focus yet there are no motile spirochetes to be found in these large areas. What gives with that?

I think that we are grossly missing something here and may be attacking the wrong form and just by chance killing the bug by attrition through its life cycle.

On the subject of membrane rupture during depressurization after HBOT, if ths where the case, one would think that there would be a herhiemer type of reaction that would start sometime after the HBOT treatment was done, possible within a few days. It would also be repeatable with each HBOT treatment.

the syphilis bacteria is in cyst form when it is in a Guma.

Lyme tends to be more in cyst form in spinal fluid and possibly bone tissue.

>>the question is how many of these other forms are floating around.

3 forms total- egg, larvae (or young adult) and adult. It is very possible that abx which has an effect on the adult forms would also have an effect on larval forms. But abx which has an effect on adult forms does not have an effect on cyst forms.

>>There MUST be lots of them and they MUST be able to convert to motile form

yeah... they grow up. Think of *insect life cycles*- it's simular.

H. pylori has a very simular life cycle and requires a combination of abx (all taken at the same time) which deal with all stages. In fact H. pylori used to be classified as a spirochete but it isn't anymore. I guess the dna is different or something. It does have a simular life cycle though.

One problem with taking combos of abx for lyme is that it's best if the bacterial load is gotten down first. Otherwise the herx could be way too much.

From what I have read, the blebs are fragments of protiens that get sqeezed off of the motile form the spirochete and occur naturally at a slow rate as well as at a very high rate when the spirchete is lysed with either an antibody or abx.

They are much much smaller than the cysts. My theory is that the blebs are the genetic mesengers that allow the spirochetes to communucate their protien structure. This would make sense as to why, when the outlayers are under attack, large numbers of blebs are shed, I would think that these would be segments of protiens that are not affected by the attack, and when they go floating around in large numbers, they get assimilated into the other spirochetes, thereby allowing them to evade desctruction???

On the other hand from what I have read, the cyst form somehow forms a capsule around spirocete. How this occurs I don't know as the cyst envelope has to be constructed from something.

It could be the result of an enzyme that stimulats the surrounding media to form a waxy protien,presumably very rich in hydrogen (cysts form in pure water so must get a significant amount of their cyst wall from either inside the spirochete or by stealing the o-h from the water molecule, a rather hard thing to do). If it is formed from the spirochete body, a significant mass loss must occur, meaning that it can only to do it a limited number of times before it can t do it any more.

Finally there is mention of L form, some papers illude that these are cyst form, yet others indicazte that they are truly a stand alone organism that are cell wall deficient. This type of thing can be produced on a microscope slide with any bacteria when the cell wall is destroyed. they just hold togeter with surface tension, like a drop of water. They are very fragile and have a limited ability to reject outside chemicals as they no longer have the cell wall to protect them. Basically they break appart easily.

The Question is does Lyme have this form and if so, is there a wall like structure but with DIFFERENT surface proteins, maybe even some that look like normal body tissue. Is it that the flagella are shed when the outer wall is lysed? then leaving only the inner wall (dontl forget that flagella fragmetn show up first in a higher propotion as compated to some of the other antigens, even with active disease.

If the inner wall is just a different wall structure with different proteins, the organism would not be detected with the current antigen probes, it would also likely be round since the flagella are gone and it may have a different metabolic function as the maximum energy consuming part of the spirochete must be the flagella which if not present don't need be be fed.

???

The terms are defined very nicely in this book. The classical form (or parent_ and the variant (sometimes called Lform S form or Cyst).

And yes- Lyme has and outer and intermediary cell wall.. with different proteins in each.

Barb

>>From what I have read, the blebs are fragments of protiens that get sqeezed off of the motile form the spirochete and occur naturally at a slow rate as well as at a very high rate when the spirchete is lysed with either an antibody or abx.

They're cyst forms- eggs. They would be composed partially of protien. Being another generation- yes, there would be genetic material passed on. & with the new stuff about spirochetes mating, then yes, of course, the material could be different from the parents.

It's fairly common in nature for some plants and animals to reproduce at a faster rate when they are stressed. Also, the cysts would fall off the spirochete when it's killed (lysed).

Your right- some cysts are smaller than others. Which makes me wonder if the larger ones could be a hibernation chamber (like a cocoon) for adults when conditions aren't very good. There is some stuff in the literature about other spirochetes remaining dormant in the body or in mud. Whether they delay hatching or hibernate is anyone's guess at this point.

Another explaination (& more likely) would be that the cysts grow larger at different stages to accomodate the growth of the baby bacteria. Here are some pictures of cysts or blebs. Especially check out the pictures on the upper left and at the bottom of the page. Really fascinating.
http://www.home.pon.net/caat/lyme/cyst_phase/cyst_phase1.html

Minocycline works for adult and maybe L forms but not for cyst forms. Flagyl, Tinidazole and hydro-something work on the cyst forms. Cell wall deficient is a little confusing to me. Cyst forms do have a wall or membrane around the eggs or larvae. I suppose technically it's not a "cell wall" though. & yes, if the membrane was disrupted before the larvae had a chance to mature fully then it would stand to reason they'd be very fragile (& hopefully DIE!!!!)

and... do you think the ceftin you took was able to get to the bones very well? I had to stop rocephin at day 28 and it wasn't done working through my bones.

Actually, the flagyl and tini seemed to do much more in my bones, but I'm counting on ceftin to kill spirochetes that may survive the cyst disruption from tini. I'm not too confident about the ceftin doing that job but it's all I have besides doxy.