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, Are you saying that all Bb is going to basically respond the

same way to all abx? With only slight variations possible?

This would certainly make it unique among bacteria and to me would

seem to make it a much easier organism to fight then, if it's that

predictable, which we certainly have not seen to be the case.

I know that people claim that in vitro testing can't always predict

what will happen in vivo, but still, it would be such a huge help,

IMO, to test your organism's sensitivity in a petri dish first,

rather than using yourself as the guinea pig. I'd rather go with the

abx that's killing a lot, than the one that's sitting there doing

nothing, or allowing the bugs to multiply.

penny

> > Whoa, really? Where? Who are they? I'd definitely be interested

in

> > looking into this. If you could culture the organisms and see

how

> they

> > respond to various abx, that would put us light years ahead when

it

> > comes to treatment.

>

> The sensitivity testing (they dont offer it but you could try

> requesting it) may be worthwhile. Because there is some variation

> between strains in natural sensitivity (I forget just how much).

>

> However, I have three papers in which Bb was isolated from the EM

> rash site both before and after treatment of EM, and MICs were

done

> for both the before-treatment isolate and the after-treatment

> isolate. In 2 of the papers, there were no changes in the MICs of

the

> drugs the organsisms had been exposed to during the therapies. In

the

> third paper the resistance gained was incremental - I think 4-fold

at

> most (seen mostly with drugs with very low MICs as I recall), and

> maybe(?) no change for some of the other patients in that study. I

> conclude that those organisms' surviving the therapy is not due to

> acquired resistance. It is due to some phenomena which have not

been

> demonstrated outside the host enviroment.

>

> THese studies were of fairly short-term therapy and after

something

> like 12 months of tx, perhaps Bb might gain more significant

acquired

> resistance to the treatment drug(s) in specific, tho I dont

> personally know of much reason to think so.

>

> http://www.focustechnologies.com/focus/1-

> reference_laboratory/search_frame.asp?f=2

>

> =========================================

>

> 51120 Borrelia burgdorferi Culture

>

> The isolation of Borrelia burgdorferi in modified Barbour-Stoenner-

> medium can be useful in confirming the diagnosis of Lyme

Disease

> in selected patients. Cultures are held for up to 4 weeks.

>

> Reference Range No Borrelia isolated

>

> Preferred Specimen Heparinized whole blood (10 mL), CSF, joint

> fluid. Skin biopsy of lesion periphery in sterile container with

> equal volume of sterile saline. " Live " tick in sterile moist

gauze.

> Transport Temperature Room temperature

> Results Available 28 to 35 days

> CPT Code 87081 Culture

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I conclude that those organisms' surviving the therapy is not due to acquired resistance. It is due to some phenomena which have not been demonstrated outside the host enviroment.

,

Bb Cysts, blebs, granules? The Brorsons' studies etc Plenty to show that spiros do have mechanisms to ensure survival under "adverse circumstances" ie in the presence of most abx in-vitro. They can then be "reborn" from their mutated forms.

In-vivo they also "flagelate" their way to sequestered sites very quickly and from there they can re-circulate and repopulate whenever they choose to.

But of course that's only hearsay, since me, myself, personally have not got my own equipment in my backroom where I can play microbiologist and then scream at people that what "I don't see(or don't know enough about!) can't "possably"(sic) make you sick".

Nelly

Nelly

[infections] borrelia culture available

> Whoa, really? Where? Who are they? I'd definitely be interested in > looking into this. If you could culture the organisms and see how they > respond to various abx, that would put us light years ahead when it > comes to treatment.The sensitivity testing (they dont offer it but you could try requesting it) may be worthwhile. Because there is some variation between strains in natural sensitivity (I forget just how much).However, I have three papers in which Bb was isolated from the EM rash site both before and after treatment of EM, and MICs were done for both the before-treatment isolate and the after-treatment isolate. In 2 of the papers, there were no changes in the MICs of the drugs the organsisms had been exposed to during the therapies. In the third paper the resistance gained was incremental - I think 4-fold at most (seen mostly with drugs with very low MICs as I recall), and maybe(?) no change for some of the other patients in that study. I conclude that those organisms' surviving the therapy is not due to acquired resistance. It is due to some phenomena which have not been demonstrated outside the host enviroment.THese studies were of fairly short-term therapy and after something like 12 months of tx, perhaps Bb might gain more significant acquired resistance to the treatment drug(s) in specific, tho I dont personally know of much reason to think so.http://www.focustechnologies.com/focus/1-reference_laboratory/search_frame.asp?f=2=========================================51120 Borrelia burgdorferi Culture The isolation of Borrelia burgdorferi in modified Barbour-Stoenner-medium can be useful in confirming the diagnosis of Lyme Disease in selected patients. Cultures are held for up to 4 weeks. Reference Range No Borrelia isolated Preferred Specimen Heparinized whole blood (10 mL), CSF, joint fluid. Skin biopsy of lesion periphery in sterile container with equal volume of sterile saline. "Live" tick in sterile moist gauze. Transport Temperature Room temperature Results Available 28 to 35 days CPT Code 87081 Culture

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Yeah, I'm not even talking about " acquired " resistance, although it

seems mind boggling to me that Bb wouldn't do what every other

bacteria does. Adapt. I'm talking about having a way to look at

which abx are most effective in vitro before GUESSING which abx to

experiment with in vivo (on humans). At least it's a starting point.

Otherwise, you've got people on Rocephin or doxy, (which for years

was the standard lyme treatment) before deciding they're not all

that effective (and getting slammed by the CDC and government in the

process).

Are the drugs effective in the petri dish? If not, I wouldn't start

with those drugs. It's not just Tony saying that the petri dish is a

good place to start. Most abx research starts there. Every

microbiologist I've talked to say it's the best place to start.

Infectious disease docs DEFINITELY utilize the petri dish in guiding

treatment. Why aren't we? Because we haven't been able to culture

the organisms, or show direct causal relationships.

We're trying to convince the-powers-that-be, that the invisible

illness we're fighting really exists based on research that the-

powers-that-be can't be bothered to read, or maybe can't comprehend.

We'd have a much stronger case to present to the government if we

could show which drugs kill Bb in the petri dish and how resistant

they are to drugs. Right now, lyme treatment is pretty much a big,

EXPENSIVE, experiment, in the CDC's view, with not much proof to

back it up. We'd be smart to rally push for something visible and

simple. Like cultures and abx sensitivities.

penny

> I

> conclude that those organisms' surviving the therapy is not due to

> acquired resistance. It is due to some phenomena which have not

been

> demonstrated outside the host enviroment.

>

> ,

>

> Bb Cysts, blebs, granules? The Brorsons' studies etc Plenty to

show that spiros do have mechanisms to ensure survival

under " adverse circumstances " ie in the presence of most abx in-

vitro. They can then be " reborn " from their mutated forms.

>

> In-vivo they also " flagelate " their way to sequestered sites very

quickly and from there they can re-circulate and repopulate whenever

they choose to.

>

> But of course that's only hearsay, since me, myself, personally

have not got my own equipment in my backroom where I can play

microbiologist and then scream at people that what " I don't see(or

don't know enough about!) can't " possably " (sic) make you sick " .

>

> Nelly

>

>

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Yes, lab studies exist which justify the typical ILADS choices of

drugs. Mouse infection studies are possibly a better model than pure

culture studies, and this paper found some very large differences

between the set of drugs that can cure a stricken mouse and the set

of drugs that can cure a stricken test tube:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=174684

Thing is, none of these mice had refractory lyme. They could all be

cured (at least for the duration of the experiment) with the right

drug, which is not what we generally see in humans. While there may

be more, I'm personally only aware of one animal ever getting

refractory lyme, and thats one dog (of 23 or something) infected by

Straubinger. A good bit of doxy failed to cure the dog.

My first guess would be that refractory lyme disease is an accident.

There is some site where Bb can lodge as a persistence form, possibly

within phagocytes, and this ability evolved to slow down eradication

by the immune systems of bird, mammal, and reptile hosts. However in

some hosts this persistence form is very poorly cleared and therefore

accumulates greatly, which does not occur in most hosts. Something

(efflux?) gives this persistence form nonspecific drug resistance

like the intraphagocytic survival forms of chlamydia in ReA. Just a

guess.

If there is a pecularity of the human immune system that allows this

sort of thing to take place, it may have been forged by selective

pressures arising from the unique lifestyle of humans. Some say

smallpox killed more humans in the historical era than all other

diseases put together, so I am trying to learn about it, but its not

that well known. Anyways it may be we have more than our fair share

of disease because of our extensive contact with sheep, chickens,

dogs, rats etc, which is unique, and alos our degree of intra-species

sociality, which is uncommon. Some say M. tuberculosis got us by way

of the cow, so domesticating the latter was possibly not an unmixed

smooth move. We may also have on average different *types* of

diseases than our mammalian ancestors, not just more. I dont think

either possiblity can be verified; we sure do know it all about human

illness patterns, but illness in mammals in nature cant be studied

well because god comes for the sick lil animals real real fast,

blammo. When I had hypoglycemic attacks last summer and couldnt think

clearly enough to find my way out of the grocery store, thats about

when I would have noticed a tiger chewing on my neck if it werent for

this whole civilization thing, and how theyre not allowed in the

grocery store.

<pennyhoule@y...> wrote:

> Yeah, I'm not even talking about " acquired " resistance, although it

> seems mind boggling to me that Bb wouldn't do what every other

> bacteria does. Adapt. I'm talking about having a way to look at

> which abx are most effective in vitro before GUESSING which abx to

> experiment with in vivo (on humans). At least it's a starting

point.

> Otherwise, you've got people on Rocephin or doxy, (which for years

> was the standard lyme treatment) before deciding they're not all

> that effective (and getting slammed by the CDC and government in

the

> process).

>

> Are the drugs effective in the petri dish? If not, I wouldn't start

> with those drugs. It's not just Tony saying that the petri dish is

a

> good place to start. Most abx research starts there. Every

> microbiologist I've talked to say it's the best place to start.

> Infectious disease docs DEFINITELY utilize the petri dish in

guiding

> treatment. Why aren't we? Because we haven't been able to culture

> the organisms, or show direct causal relationships.

>

> We're trying to convince the-powers-that-be, that the invisible

> illness we're fighting really exists based on research that the-

> powers-that-be can't be bothered to read, or maybe can't

comprehend.

> We'd have a much stronger case to present to the government if we

> could show which drugs kill Bb in the petri dish and how resistant

> they are to drugs. Right now, lyme treatment is pretty much a big,

> EXPENSIVE, experiment, in the CDC's view, with not much proof to

> back it up. We'd be smart to rally push for something visible and

> simple. Like cultures and abx sensitivities.

>

> penny

>

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Nelly

Bacteria don't have a brain they just respond to chemical

scenario's. I would think your cells and other factors are

responsable for what they are or ain't capable of doing.It's not

like they jump into a corner of your stomach to avoid something-THEY

CAN " T THINK.Bacteria once there requirements are met start to

multiply and the more fuel they have the more they can multiply.They

are very fickle organisms and can only respond to SCENARIO " S not

think and move, just basically the laws of nature.Also some really

bad bugs like streptococcus can't stick to anything but the

throat.If I tenderised your leg and fed you toxins to make your

cells more bacteria friendly you can get bad bacteria sticking and

causing damage away from there designated sites.

> OK, if you say so, but spiros do " move " (spiral?) their way into

whatever they elect as an interesting and sheltered area.

>

> Nelly

> [infections] Re: borrelia culture

available

>

>

> Hi Nelly

> What your describing as flagella in your spirochetes, is not

> flagella, it only looks like flagella, it's unwinding of strands

off

> the spirochete. Just happened to notice that one in my

microbiology

> books.

> thanks tony

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" Barb Peck " <egroups1bp@y...> wrote:

A resistant strain has MUTATED genetically to resist a ceretain abx

> forever - but it remains in it's classical form

Actually, I think that's a widely made assumption that's not really

proven, that once resistance is acquired, the bugs are permanently

resistant due to genetic mutation. There ARE a few studies I " ve

seen, and some scientists & microbiologists HAVE observed, and

patients HAVE reported, and even our very own Hagrid, er, I mean

Tony (who's hobby and passion happens to be playing with nasty

bacteria) that organisms develop resistance to an antibiotic, but

after some months will sometimes become sensitive to it again, both

in vivo and in vitro. So, this may support some of what is

saying in some way, that there's some other mechanism at work

besides pure antibiotic resistance being acquired.

penny

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