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Actually, some MDs are able to do lab research. So this picture is not

quite accurate.

The most amazing thing is, weve got the Nobel committee saying RA and

Crohn's could be bacterial infections, and literally or virtually no

one is publishing on how such bacteria might be resisting

chemotherapeutic eradication. We need to not just investigate cryptic

bacteria, we need to investigate how to blow them to hell.

> Highly educated, highly acute people like Ewald and

> Wheldon can sound off with all intelligence and scholarship about

> these ideas until the cows come home, but their effect on what

> experiments get done is limited unless and until research professors

> decide to risk their careers on whether they can convince NIH, etc,

> that this stuff deserves large investments despite being the

opposite

> of the theories everyone learned in school.

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This is true. I just had an exhausting long conversation with a woman-

-and I'm on amoxicillin and feeling very tense and weird from the abx

as I hate abx--but I self prescribed it after extracting the tooth

I'd been posting about a few weeks earlier--anyhoo---

I spent like a fricken HOUR trying to explain that yes she has

rheumatoid arthritis but since she did have lyme disease and took abx

for 2 years for it, she still has lyme. She is on powerful

immunosuppressive drugs that are affecting her liver and white blood

count but lives an active life with her husband being photographers

and going to asia and nepal and so on a few times a year to publish

books of pictures etc. So I told her, look, I'm not questioning what

you're doing, lyme is not really curable, but you need to understand

what's going on. I'm fricken IRRITABLE and exhausted which partly

explains my emial to you but honestly I can't hel pyou anyway. She

kept saying, but I need to live life now, what else can I do, and my

doctor says I did have lyme but now I have r.a. and the lyme

triggered it and the lyme is gone nad I said no I stake my life on

the fact you still have lyme; I said genes activity depends on the

signals from the environment, there aren't hit and run drivers, you

don't just meet a pathogen and it goes on its merry way and forever

and ever your immune system attacks itself, NO. I said I don't

quesiton your decision you're travelling to asia and having a career

but you need to understand what is really going on in your body and

also understand there are consequences to your choice, immune

suppression can lead to cancer and liver problmes and so on and its a

risk tho not a guarantee but you need to be aware of that.

It took a lot of exhausting insistence on my part to get through and

I don't know why I do this, why do I do this? She's doing better than

me if she can travel to Asia, I couldn't have the stamina for that

now. Neither would I be making her choice but I understand her choice.

She said but lots of people have r.a. and don't hav elyme and I said

sure but they have some kind of chronic infection.

I said look at ulcers--there's your model, its the same model, and he

just won the Nobel. I said, treat the symptoms and the inflammation

keeps coming back. Treat the pathogen and it goes away.

I don't know if we CAN eradicate these pathogens completely. I'm

not sure if its possible. Maybe if we can lower their #'s enough even

those of us with the suscpetible inflammatory genes will be okay. I

really don't know. I suspect the inflammation perpetuates the

infection yet keeps it in check (the mice with th eknockout genes got

sicker than the mice with the inflammatory genes in lyme experiments)

in some way. I'm not sure the answer will be found anytime soon.

Why did I do this I don't know. I should've just been pleasant and

said I'm so sorry you got r.a., and I should never have indulged in

this long conversation. Then she asked, do you have someone to

advocate for you, if you end up in the hospital or make an incorrect

decision? And I said no. I'd explained to her that I was so sick of

all the bad decisions docs had made my whole life that I would never

let anybody direct my care ever again, and nobody is as smart as me

about my situation so it's just me. She didn't think that was wise.

>

>

> Actually, some MDs are able to do lab research. So this picture is

not

> quite accurate.

>

> The most amazing thing is, weve got the Nobel committee saying RA

and

> Crohn's could be bacterial infections, and literally or virtually

no

> one is publishing on how such bacteria might be resisting

> chemotherapeutic eradication. We need to not just investigate

cryptic

> bacteria, we need to investigate how to blow them to hell.

>

> > Highly educated, highly acute people like Ewald and

> > Wheldon can sound off with all intelligence and scholarship about

> > these ideas until the cows come home, but their effect on what

> > experiments get done is limited unless and until research

professors

> > decide to risk their careers on whether they can convince NIH,

etc,

> > that this stuff deserves large investments despite being the

> opposite

> > of the theories everyone learned in school.

>

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Good luck with your abx eating.

These bacteria have almost all the same ribosomal targets, the same

enzymatic targets, all the same drug targets as an E. coli bladder

infection has. Ergo, either

A. bacteriostasis due to drugs does not cause them to be eliminated by

the host (somewhat unlikely), or

B. bacteriostasis due to drugs is an elective stress response that

doesnt occur in all bacteria in all circumstances (rather unlikely), or

C. the drugs arent getting to their targets, for some particular

molecular reason. Which is what I've focused on.

Its not necessarily some impenetrable mystery. As of now theres no

particular reason to suspect that it probably cant be solved.

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Biofilms, maybe in some cases.

Evolution thru selective pressure in other cases. I've been reading

up on amoxicillin today out of curiosity. In chornic lyme they say 6

grams a day, I'm doing 1.5 grams yesterday and today. Anyway, as you

know, they created augmentin becuase some bacteria became resistant

to amoxy

>

> Good luck with your abx eating.

>

> These bacteria have almost all the same ribosomal targets, the same

> enzymatic targets, all the same drug targets as an E. coli bladder

> infection has. Ergo, either

>

> A. bacteriostasis due to drugs does not cause them to be eliminated

by

> the host (somewhat unlikely), or

>

> B. bacteriostasis due to drugs is an elective stress response that

> doesnt occur in all bacteria in all circumstances (rather

unlikely), or

>

> C. the drugs arent getting to their targets, for some particular

> molecular reason. Which is what I've focused on.

>

> Its not necessarily some impenetrable mystery. As of now theres no

> particular reason to suspect that it probably cant be solved.

>

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On Sunday, October 30, 2005, at 03:38 PM, jill1313 wrote:

> I spent like a fricken HOUR trying to explain that yes she has

> rheumatoid arthritis but since she did have lyme disease and took abx

> for 2 years for it, she still has lyme....

> It took a lot of exhausting insistence on my part to get through and

> I don't know why I do this, why do I do this? She's doing better than

> me if she can travel to Asia, I couldn't have the stamina for that

> now. Neither would I be making her choice but I understand her choice.

Jill, you do this because you're an empathetic person and you don't

want to see complete disaster happen to this person. I don't know if

I've ever spent an hour trying to convince someone who wasn't open to

it, but I sure do at least try to leave hints that people might think

about!

- Kate

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Thanx Kate.

I should only do it when someone asks.

If someone has elected powerful immunosuppressive drugs they ain't

gonna listen to me. I would've been better off working!

>

> > I spent like a fricken HOUR trying to explain that yes she has

> > rheumatoid arthritis but since she did have lyme disease and took

abx

> > for 2 years for it, she still has lyme....

> > It took a lot of exhausting insistence on my part to get through

and

> > I don't know why I do this, why do I do this? She's doing better

than

> > me if she can travel to Asia, I couldn't have the stamina for that

> > now. Neither would I be making her choice but I understand her

choice.

>

> Jill, you do this because you're an empathetic person and you don't

> want to see complete disaster happen to this person. I don't know

if

> I've ever spent an hour trying to convince someone who wasn't open

to

> it, but I sure do at least try to leave hints that people might

think

> about!

>

> - Kate

>

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> Biofilms, maybe in some cases.

True.

> Evolution thru selective pressure in other cases.

I dont think this is an important factor, at least not on on a month-

to-month scale:

==========================

Antimicrob Agents Chemother. 2005 Apr;49(4):1294-301.

In vitro susceptibility testing of Borrelia burgdorferi sensu lato

isolates cultured from patients with erythema migrans before and

after antimicrobial chemotherapy.

Hunfeld KP, Ruzic-Sabljic E, Norris DE, Kraiczy P, Strle F.

Institute of Medical Microbiology, University Hospital of furt,

-Ehrlich Str. 40, D-60596 furt/Main, Germany.

K.Hunfeld@...

Clinical treatment failures have been reported to occur in early Lyme

borreliosis (LB) for many suitable antimicrobial agents.

Investigations of possible resistance mechanisms of the Borrelia

burgdorferi complex must analyze clinical isolates obtained from LB

patients, despite their receiving antibiotic treatment. Here,

borrelial isolates obtained from five patients with erythema migrans

(EM) before the start of antibiotic therapy and again after the

conclusion of treatment were investigated. The 10 isolates were

characterized by restriction fragment length polymorphism analysis

and plasmid profile analysis and subjected to susceptibility testing

against a variety of antimicrobial agents including those used for

initial chemotherapy. Four out of five patients were infected by the

same genospecies (Borrelia afzelii, n = 3; Borrelia garinii, n = 1)

at the site of the EM lesion before and after antimicrobial therapy.

In one patient the genospecies of the initial isolate (B. afzelii)

differed from that of the follow-up isolate (B. garinii). No

significant changes in the in vitro susceptibilities became obvious

for corresponding clinical isolates before the start and after the

conclusion of antimicrobial therapy. This holds true for the

antimicrobial agents used for specific chemotherapy of the patients,

as well as for any of the additional agents tested in vitro. Our

study substantiates borrelial persistence in some EM patients at the

site of the infectious lesion despite antibiotic treatment over a

reasonable time period. Borrelial persistence, however, was not

caused by increasing MICs or minimal borreliacidal concentrations in

these isolates. Therefore, resistance mechanisms other than acquired

resistance to antimicrobial agents should be considered in patients

with LB resistant to treatment.

Publication Types:

Clinical Trial

PMID: 15793100 [PubMed - indexed for MEDLINE]

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Maybe. They're basically suggesting immune deficiency on the part of

the patient, I suppose.

Personally selective pressure makes sense to me, then of course there

is genetics but if you're generally saying we're having trouble

eradicating bugs and we know there is antibiotic overuse and MSRA for

example, why would you not favor selective pressure. As

e said to me with borrelia you'relooking at a million years of

evolution compressed into one moment. Its spent a long time figuring

out how to evade whatever wants to kill it.

>

>

> > Biofilms, maybe in some cases.

>

> True.

>

> > Evolution thru selective pressure in other cases.

>

> I dont think this is an important factor, at least not on on a

month-

> to-month scale:

>

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

>

> Antimicrob Agents Chemother. 2005 Apr;49(4):1294-301.

>

> In vitro susceptibility testing of Borrelia burgdorferi sensu lato

> isolates cultured from patients with erythema migrans before and

> after antimicrobial chemotherapy.

>

> Hunfeld KP, Ruzic-Sabljic E, Norris DE, Kraiczy P, Strle F.

>

> Institute of Medical Microbiology, University Hospital of

furt,

> -Ehrlich Str. 40, D-60596 furt/Main, Germany.

> K.Hunfeld@e...

>

> Clinical treatment failures have been reported to occur in early

Lyme

> borreliosis (LB) for many suitable antimicrobial agents.

> Investigations of possible resistance mechanisms of the Borrelia

> burgdorferi complex must analyze clinical isolates obtained from LB

> patients, despite their receiving antibiotic treatment. Here,

> borrelial isolates obtained from five patients with erythema

migrans

> (EM) before the start of antibiotic therapy and again after the

> conclusion of treatment were investigated. The 10 isolates were

> characterized by restriction fragment length polymorphism analysis

> and plasmid profile analysis and subjected to susceptibility

testing

> against a variety of antimicrobial agents including those used for

> initial chemotherapy. Four out of five patients were infected by

the

> same genospecies (Borrelia afzelii, n = 3; Borrelia garinii, n = 1)

> at the site of the EM lesion before and after antimicrobial

therapy.

> In one patient the genospecies of the initial isolate (B. afzelii)

> differed from that of the follow-up isolate (B. garinii). No

> significant changes in the in vitro susceptibilities became obvious

> for corresponding clinical isolates before the start and after the

> conclusion of antimicrobial therapy. This holds true for the

> antimicrobial agents used for specific chemotherapy of the

patients,

> as well as for any of the additional agents tested in vitro. Our

> study substantiates borrelial persistence in some EM patients at

the

> site of the infectious lesion despite antibiotic treatment over a

> reasonable time period. Borrelial persistence, however, was not

> caused by increasing MICs or minimal borreliacidal concentrations

in

> these isolates. Therefore, resistance mechanisms other than

acquired

> resistance to antimicrobial agents should be considered in patients

> with LB resistant to treatment.

>

> Publication Types:

> Clinical Trial

>

> PMID: 15793100 [PubMed - indexed for MEDLINE]

>

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Its possible that when they sample the patient after treatment,

genetically-resistant bacterial individuals are totally outcompeted

in the culture by wild-type individuals, and vanish from the culture.

This could explain why genetically-resistant individuals are not seen.

I think its more likely that such individuals are not seen because

they arent there - and the resistance within the host is phenotypic.

These authors seem to agree. It would be interesting to recover

Tropheryma whipplei from drug-refractory cases and see if these bugs

are drug sensitive in glass. I'd expect they would be.

This author just spoke at ILADS/LDA this weekend, I hope we will

eventually find out what he said.

<jenbooks13@h...> wrote:

>

> Maybe. They're basically suggesting immune deficiency on the part

of

> the patient, I suppose.

>

> Personally selective pressure makes sense to me, then of course

there

> is genetics but if you're generally saying we're having trouble

> eradicating bugs and we know there is antibiotic overuse and MSRA

for

> example, why would you not favor selective pressure. As

> e said to me with borrelia you'relooking at a million years

of

> evolution compressed into one moment. Its spent a long time

figuring

> out how to evade whatever wants to kill it.

>

>

> >

> >

> > > Biofilms, maybe in some cases.

> >

> > True.

> >

> > > Evolution thru selective pressure in other cases.

> >

> > I dont think this is an important factor, at least not on on a

> month-

> > to-month scale:

> >

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

> >

> > Antimicrob Agents Chemother. 2005 Apr;49(4):1294-301.

> >

> > In vitro susceptibility testing of Borrelia burgdorferi sensu

lato

> > isolates cultured from patients with erythema migrans before and

> > after antimicrobial chemotherapy.

> >

> > Hunfeld KP, Ruzic-Sabljic E, Norris DE, Kraiczy P, Strle F.

> >

> > Institute of Medical Microbiology, University Hospital of

> furt,

> > -Ehrlich Str. 40, D-60596 furt/Main, Germany.

> > K.Hunfeld@e...

> >

> > Clinical treatment failures have been reported to occur in early

> Lyme

> > borreliosis (LB) for many suitable antimicrobial agents.

> > Investigations of possible resistance mechanisms of the Borrelia

> > burgdorferi complex must analyze clinical isolates obtained from

LB

> > patients, despite their receiving antibiotic treatment. Here,

> > borrelial isolates obtained from five patients with erythema

> migrans

> > (EM) before the start of antibiotic therapy and again after the

> > conclusion of treatment were investigated. The 10 isolates were

> > characterized by restriction fragment length polymorphism

analysis

> > and plasmid profile analysis and subjected to susceptibility

> testing

> > against a variety of antimicrobial agents including those used

for

> > initial chemotherapy. Four out of five patients were infected by

> the

> > same genospecies (Borrelia afzelii, n = 3; Borrelia garinii, n =

1)

> > at the site of the EM lesion before and after antimicrobial

> therapy.

> > In one patient the genospecies of the initial isolate (B.

afzelii)

> > differed from that of the follow-up isolate (B. garinii). No

> > significant changes in the in vitro susceptibilities became

obvious

> > for corresponding clinical isolates before the start and after

the

> > conclusion of antimicrobial therapy. This holds true for the

> > antimicrobial agents used for specific chemotherapy of the

> patients,

> > as well as for any of the additional agents tested in vitro. Our

> > study substantiates borrelial persistence in some EM patients at

> the

> > site of the infectious lesion despite antibiotic treatment over a

> > reasonable time period. Borrelial persistence, however, was not

> > caused by increasing MICs or minimal borreliacidal concentrations

> in

> > these isolates. Therefore, resistance mechanisms other than

> acquired

> > resistance to antimicrobial agents should be considered in

patients

> > with LB resistant to treatment.

> >

> > Publication Types:

> > Clinical Trial

> >

> > PMID: 15793100 [PubMed - indexed for MEDLINE]

> >

>

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What author?

> > >

> > >

> > > > Biofilms, maybe in some cases.

> > >

> > > True.

> > >

> > > > Evolution thru selective pressure in other cases.

> > >

> > > I dont think this is an important factor, at least not on on a

> > month-

> > > to-month scale:

> > >

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

> > >

> > > Antimicrob Agents Chemother. 2005 Apr;49(4):1294-301.

> > >

> > > In vitro susceptibility testing of Borrelia burgdorferi sensu

> lato

> > > isolates cultured from patients with erythema migrans before

and

> > > after antimicrobial chemotherapy.

> > >

> > > Hunfeld KP, Ruzic-Sabljic E, Norris DE, Kraiczy P, Strle F.

> > >

> > > Institute of Medical Microbiology, University Hospital of

> > furt,

> > > -Ehrlich Str. 40, D-60596 furt/Main, Germany.

> > > K.Hunfeld@e...

> > >

> > > Clinical treatment failures have been reported to occur in

early

> > Lyme

> > > borreliosis (LB) for many suitable antimicrobial agents.

> > > Investigations of possible resistance mechanisms of the

Borrelia

> > > burgdorferi complex must analyze clinical isolates obtained

from

> LB

> > > patients, despite their receiving antibiotic treatment. Here,

> > > borrelial isolates obtained from five patients with erythema

> > migrans

> > > (EM) before the start of antibiotic therapy and again after the

> > > conclusion of treatment were investigated. The 10 isolates were

> > > characterized by restriction fragment length polymorphism

> analysis

> > > and plasmid profile analysis and subjected to susceptibility

> > testing

> > > against a variety of antimicrobial agents including those used

> for

> > > initial chemotherapy. Four out of five patients were infected

by

> > the

> > > same genospecies (Borrelia afzelii, n = 3; Borrelia garinii, n

=

> 1)

> > > at the site of the EM lesion before and after antimicrobial

> > therapy.

> > > In one patient the genospecies of the initial isolate (B.

> afzelii)

> > > differed from that of the follow-up isolate (B. garinii). No

> > > significant changes in the in vitro susceptibilities became

> obvious

> > > for corresponding clinical isolates before the start and after

> the

> > > conclusion of antimicrobial therapy. This holds true for the

> > > antimicrobial agents used for specific chemotherapy of the

> > patients,

> > > as well as for any of the additional agents tested in vitro.

Our

> > > study substantiates borrelial persistence in some EM patients

at

> > the

> > > site of the infectious lesion despite antibiotic treatment over

a

> > > reasonable time period. Borrelial persistence, however, was not

> > > caused by increasing MICs or minimal borreliacidal

concentrations

> > in

> > > these isolates. Therefore, resistance mechanisms other than

> > acquired

> > > resistance to antimicrobial agents should be considered in

> patients

> > > with LB resistant to treatment.

> > >

> > > Publication Types:

> > > Clinical Trial

> > >

> > > PMID: 15793100 [PubMed - indexed for MEDLINE]

> > >

> >

>

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Great study find! You'd think this one would really sum up the problem

and researchers would start looking to answer the right question. Maybe

that's a bit much to hope for though. Probably it will barely be

noticed, if at all, by the people that need to see it.

- Kate

On Sunday, October 30, 2005, at 05:20 PM, wrote:

> Antimicrob Agents Chemother. 2005 Apr;49(4):1294-301.

>  

> In vitro susceptibility testing of Borrelia burgdorferi sensu lato

> isolates cultured from patients with erythema migrans before and

> after antimicrobial chemotherapy.

>

> Hunfeld KP, Ruzic-Sabljic E, Norris DE, Kraiczy P, Strle F.

and

> C. the drugs arent getting to their targets, for some particular

> molecular reason. Which is what I've focused on.

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There are two other studies with similar results... at least one of

them is about 10 years old.

>

> Great study find! You'd think this one would really sum up the

problem

> and researchers would start looking to answer the right question.

Maybe

> that's a bit much to hope for though. Probably it will barely be

> noticed, if at all, by the people that need to see it.

>

> - Kate

>

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Hi Jill, do you have a reference for the Amoxy dosages you mention?

I have been taking it now or several weeks. I took 200mg per day and

it wasn't enough I had too much pain. When I ramped up to 300mg per

day I felt better. Had to stop last week because I couldn't afford to

buy it and was miserable and lost all last week to pain and sleep.

Also, I hear some take Ketek or something along with Amoxy to help it

along. Do you have any iea what that is, and the dosage? My

understanding is that Ketek reduces the amount of Amoxy needed.

Thanks for any info you may have, Hope you feel better soon.

*S*

> >

> > Good luck with your abx eating.

> >

> > These bacteria have almost all the same ribosomal targets, the

same

> > enzymatic targets, all the same drug targets as an E. coli

bladder

> > infection has. Ergo, either

> >

> > A. bacteriostasis due to drugs does not cause them to be

eliminated

> by

> > the host (somewhat unlikely), or

> >

> > B. bacteriostasis due to drugs is an elective stress response

that

> > doesnt occur in all bacteria in all circumstances (rather

> unlikely), or

> >

> > C. the drugs arent getting to their targets, for some particular

> > molecular reason. Which is what I've focused on.

> >

> > Its not necessarily some impenetrable mystery. As of now theres

no

> > particular reason to suspect that it probably cant be solved.

> >

>

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Wait a sec. 200 mg a day??? Thats not possible it comes in 500 mg

capsules. Or do you mean 2000 mg a day? And then 3000 mg a day.

Go to drugstore.com. You can get 150, 500 mg capsules for about $25

or $30. So lets see, at 3000 mg a day that would be 6 capsules a day.

So 150 capsules would last...25 days. So the cost for month can't be

more than about $35 for 3000 mg/day. Can you afford that?

I have those refs just asking around. I re-read Art Doherty (6 grams

a day) and asked on lymenet--they did as low as 4 grams a day and as

high as 24 grams a day....ay yay yay.

Today I did 2 grams and before bed I may take one more so 2.5 grams.

It may be thats my max for now. Maybe 500 mg morning, afternoon, and

then 1000 before bed. It whacks me out and at the same time I feel it

attacking slyme symptoms.

The weird thing is, ever since I took it (I premedicated for my tooth

on Friday) I have had an intense craving for milk and cheese. I mean,

I have scarfed down more cheese than you can believe. And I don't

want my veggies at all...my green juices etc seem unpalatable to me.

Usually I eat a lot of veggies. And as soon as I got out of the

dentist I made a beeline to a small store to get milk and drank it

down. THen I bought milk over the weekend. Can't remember the last

time I drank store bought milk. Maybe a decade or two ago?

Now what is THAT about? That is weird.

> > >

> > > Good luck with your abx eating.

> > >

> > > These bacteria have almost all the same ribosomal targets, the

> same

> > > enzymatic targets, all the same drug targets as an E. coli

> bladder

> > > infection has. Ergo, either

> > >

> > > A. bacteriostasis due to drugs does not cause them to be

> eliminated

> > by

> > > the host (somewhat unlikely), or

> > >

> > > B. bacteriostasis due to drugs is an elective stress response

> that

> > > doesnt occur in all bacteria in all circumstances (rather

> > unlikely), or

> > >

> > > C. the drugs arent getting to their targets, for some

particular

> > > molecular reason. Which is what I've focused on.

> > >

> > > Its not necessarily some impenetrable mystery. As of now theres

> no

> > > particular reason to suspect that it probably cant be solved.

> > >

> >

>

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yer right. 500 mg X 4 a day, when I increased to X6 per day I felt

better.

Sorry, brain slime.

*S*

> > > >

> > > > Good luck with your abx eating.

> > > >

> > > > These bacteria have almost all the same ribosomal targets,

the

> > same

> > > > enzymatic targets, all the same drug targets as an E. coli

> > bladder

> > > > infection has. Ergo, either

> > > >

> > > > A. bacteriostasis due to drugs does not cause them to be

> > eliminated

> > > by

> > > > the host (somewhat unlikely), or

> > > >

> > > > B. bacteriostasis due to drugs is an elective stress response

> > that

> > > > doesnt occur in all bacteria in all circumstances (rather

> > > unlikely), or

> > > >

> > > > C. the drugs arent getting to their targets, for some

> particular

> > > > molecular reason. Which is what I've focused on.

> > > >

> > > > Its not necessarily some impenetrable mystery. As of now

theres

> > no

> > > > particular reason to suspect that it probably cant be solved.

> > > >

> > >

> >

>

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Yes, about the cheese and milk thing - me too. Bought some good

cheese last week and have been making cheese crisps.

Also craving peanut butter. Actually made a peanut butter and banana

sandwich. Haven't had that in DECADES.

The Amoxy I take is compounded. $80 for 60 capsules. No dyes.

Cheers and thx,

*S*

*S*

> > > >

> > > > Good luck with your abx eating.

> > > >

> > > > These bacteria have almost all the same ribosomal targets,

the

> > same

> > > > enzymatic targets, all the same drug targets as an E. coli

> > bladder

> > > > infection has. Ergo, either

> > > >

> > > > A. bacteriostasis due to drugs does not cause them to be

> > eliminated

> > > by

> > > > the host (somewhat unlikely), or

> > > >

> > > > B. bacteriostasis due to drugs is an elective stress response

> > that

> > > > doesnt occur in all bacteria in all circumstances (rather

> > > unlikely), or

> > > >

> > > > C. the drugs arent getting to their targets, for some

> particular

> > > > molecular reason. Which is what I've focused on.

> > > >

> > > > Its not necessarily some impenetrable mystery. As of now

theres

> > no

> > > > particular reason to suspect that it probably cant be solved.

> > > >

> > >

> >

>

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Sue if it helped you I'd go generic, drugstore.com. There are many

meds I can't take, esp. tablets I avoid like the dickens, but I don't

think regular amoxicillin has too much thats bad in it. I checked:

Inactive ingredients: D & C Red No. 28, FD & C Blue No. 1, FD & C Red

No. 40, gelatin, magnesium stearate, and titanium dioxide.

Gelatin is the capsule, not much you can do about that. THe other

ingredients really aren't too bad when you consider how little you're

getting unless you're hugely chemically sensitive. Otherwise you are

going to find the price wayyyyy too exorbitant I agree.

I avoid maltodextrin--and Yasko's work shows that in chronic

infection you avoid that because of glutamate excitoxicity. In fact,

I didn't know why but I know I can't handle it and the sleeping pills

(temezapem) I only get from one company, which is at one drugstore in

my neighborhood, because they use lactose as a filler, not

maltodextrin.

I think you'd be okay with generic but I don't know your whole

history. Seems like bacteria are more dangerous than a smidge of dye.

I don't get the cravings. Its not fat in particular, its dairy.

> > > > >

> > > > > Good luck with your abx eating.

> > > > >

> > > > > These bacteria have almost all the same ribosomal targets,

> the

> > > same

> > > > > enzymatic targets, all the same drug targets as an E. coli

> > > bladder

> > > > > infection has. Ergo, either

> > > > >

> > > > > A. bacteriostasis due to drugs does not cause them to be

> > > eliminated

> > > > by

> > > > > the host (somewhat unlikely), or

> > > > >

> > > > > B. bacteriostasis due to drugs is an elective stress

response

> > > that

> > > > > doesnt occur in all bacteria in all circumstances (rather

> > > > unlikely), or

> > > > >

> > > > > C. the drugs arent getting to their targets, for some

> > particular

> > > > > molecular reason. Which is what I've focused on.

> > > > >

> > > > > Its not necessarily some impenetrable mystery. As of now

> theres

> > > no

> > > > > particular reason to suspect that it probably cant be

solved.

> > > > >

> > > >

> > >

> >

>

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P.S. How do you make a cheese crisp.\ THat sounds good.-

-- In infections , " Sue "

<invisigyrl@y...> wrote:

>

> Yes, about the cheese and milk thing - me too. Bought some good

> cheese last week and have been making cheese crisps.

> Also craving peanut butter. Actually made a peanut butter and

banana

> sandwich. Haven't had that in DECADES.

> The Amoxy I take is compounded. $80 for 60 capsules. No dyes.

> Cheers and thx,

> *S*

> *S*

>

>

>

> > > > >

> > > > > Good luck with your abx eating.

> > > > >

> > > > > These bacteria have almost all the same ribosomal targets,

> the

> > > same

> > > > > enzymatic targets, all the same drug targets as an E. coli

> > > bladder

> > > > > infection has. Ergo, either

> > > > >

> > > > > A. bacteriostasis due to drugs does not cause them to be

> > > eliminated

> > > > by

> > > > > the host (somewhat unlikely), or

> > > > >

> > > > > B. bacteriostasis due to drugs is an elective stress

response

> > > that

> > > > > doesnt occur in all bacteria in all circumstances (rather

> > > > unlikely), or

> > > > >

> > > > > C. the drugs arent getting to their targets, for some

> > particular

> > > > > molecular reason. Which is what I've focused on.

> > > > >

> > > > > Its not necessarily some impenetrable mystery. As of now

> theres

> > > no

> > > > > particular reason to suspect that it probably cant be

solved.

> > > > >

> > > >

> > >

> >

>

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On Monday, October 31, 2005, at 09:23 PM, jill1313 wrote:

> I have those refs just asking around. I re-read Art Doherty (6 grams

> a day) and asked on lymenet--they did as low as 4 grams a day and as

> high as 24 grams a day....ay yay yay.

>

Burrascano says for Lyme: *Amoxicillin- Adults: 1g q8h plus probenecid

500mg q8h; doses up to 6 grams daily are

often needed

The probenecid is supposed to keep the levels of Amoxicillin higher --

keep it from leaving the body.

- Kate

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Im' a less-is-more gal. I don't want to mix in extra stuff. I might

even go to penicillin at some point. I mean, theoretically I should

be taking augmentin at least in part along with amoxy because I

figure I probably have coagaluase negative staph...just seeing how my

sinuses and bladder are reacting (well) to this. But I think KISS,

keep it simple. Yeah it keeps it in the blood longer but borrelia

ain't in the blood much anyway.

>

> > I have those refs just asking around. I re-read Art Doherty (6

grams

> > a day) and asked on lymenet--they did as low as 4 grams a day and

as

> > high as 24 grams a day....ay yay yay.

> >

>

> Burrascano says for Lyme: *Amoxicillin- Adults: 1g q8h plus

probenecid

> 500mg q8h; doses up to 6 grams daily are

> often needed

>

> The probenecid is supposed to keep the levels of Amoxicillin

higher --

> keep it from leaving the body.

>

> - Kate

>

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> Yeah it keeps it in the blood longer but borrelia

> ain't in the blood much anyway.

I wouldnt be so sure.

Also, the concentration of a drug in the blood largely determines the

concentrations in tissues. A co-drug that slows elimination of an

antibacterial drug will affect concentrations in the whole body, not

just the blood.

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I've read that paper several times.

It's got alot of information in there.

It's interesting that they peg the % of people that don't respond

favorably to abx in the long term so low. I'd really like to know

what that number TRULY is. I know I'm one of the few excellent

responders to abx treatment that reamins on these lists.

One thing that's really interesting in that paper is that different

patients required different MICS of the same drug to act upon their

borrelia cultures. This was in vitro if I remember correctly, so it

can't be individual differences in drug metabolism.

So it might host/pathogen adaptation.

I'm not sure how they're using the term selective pressure- I

suppose that could be from the persons immune system- or from drugs-

either way these bugs have been around a long time, and have many

mechanisms of survival that I'm sure they turn on depending on the

hosts defences.

All I know is that I started Lyme treatment very very symptomatic-

PCR positive for Lyme with absolutely NO IgG or IgM antibodies at

all, meaing the pathogen was definitely in control of the host.

My treatment turned that around. My 2004 test showed a marked

increase in Lyme antibodies. (2005 test will be back in 2 weeks).

Man. I think they have GOT to figure out some accurate markers of

how to track whether one is making progress or not. Other wise it

just seems it's a perpetual guessing game.

Barb

> >

> >

> > > Biofilms, maybe in some cases.

> >

> > True.

> >

> > > Evolution thru selective pressure in other cases.

> >

> > I dont think this is an important factor, at least not on on a

> month-

> > to-month scale:

> >

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

> >

> > Antimicrob Agents Chemother. 2005 Apr;49(4):1294-301.

> >

> > In vitro susceptibility testing of Borrelia burgdorferi sensu

lato

> > isolates cultured from patients with erythema migrans before and

> > after antimicrobial chemotherapy.

> >

> > Hunfeld KP, Ruzic-Sabljic E, Norris DE, Kraiczy P, Strle F.

> >

> > Institute of Medical Microbiology, University Hospital of

> furt,

> > -Ehrlich Str. 40, D-60596 furt/Main, Germany.

> > K.Hunfeld@e...

> >

> > Clinical treatment failures have been reported to occur in early

> Lyme

> > borreliosis (LB) for many suitable antimicrobial agents.

> > Investigations of possible resistance mechanisms of the Borrelia

> > burgdorferi complex must analyze clinical isolates obtained from

LB

> > patients, despite their receiving antibiotic treatment. Here,

> > borrelial isolates obtained from five patients with erythema

> migrans

> > (EM) before the start of antibiotic therapy and again after the

> > conclusion of treatment were investigated. The 10 isolates were

> > characterized by restriction fragment length polymorphism

analysis

> > and plasmid profile analysis and subjected to susceptibility

> testing

> > against a variety of antimicrobial agents including those used

for

> > initial chemotherapy. Four out of five patients were infected by

> the

> > same genospecies (Borrelia afzelii, n = 3; Borrelia garinii, n =

1)

> > at the site of the EM lesion before and after antimicrobial

> therapy.

> > In one patient the genospecies of the initial isolate (B.

afzelii)

> > differed from that of the follow-up isolate (B. garinii). No

> > significant changes in the in vitro susceptibilities became

obvious

> > for corresponding clinical isolates before the start and after

the

> > conclusion of antimicrobial therapy. This holds true for the

> > antimicrobial agents used for specific chemotherapy of the

> patients,

> > as well as for any of the additional agents tested in vitro. Our

> > study substantiates borrelial persistence in some EM patients at

> the

> > site of the infectious lesion despite antibiotic treatment over a

> > reasonable time period. Borrelial persistence, however, was not

> > caused by increasing MICs or minimal borreliacidal concentrations

> in

> > these isolates. Therefore, resistance mechanisms other than

> acquired

> > resistance to antimicrobial agents should be considered in

patients

> > with LB resistant to treatment.

> >

> > Publication Types:

> > Clinical Trial

> >

> > PMID: 15793100 [PubMed - indexed for MEDLINE]

> >

>

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Well I would be so sure or it would be easy to view on blood smears.

Besides it likes tissue, haven't you read all the literature?

Time for you to go to grad school and get down into bench science and

make some concrete discoveries. Too much speculation.

>

> > Yeah it keeps it in the blood longer but borrelia

> > ain't in the blood much anyway.

>

> I wouldnt be so sure.

>

> Also, the concentration of a drug in the blood largely determines

the

> concentrations in tissues. A co-drug that slows elimination of an

> antibacterial drug will affect concentrations in the whole body, not

> just the blood.

>

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Barb, it also just might be the strain. Different strains exhibit

relative resistance to drugs, at higher levels, they succumb.

>

> So it might host/pathogen adaptation.

>

> I'm not sure how they're using the term selective pressure- I

> suppose that could be from the persons immune system- or from drugs-

> either way these bugs have been around a long time, and have many

> mechanisms of survival that I'm sure they turn on depending on the

> hosts defences.

>

> All I know is that I started Lyme treatment very very symptomatic-

> PCR positive for Lyme with absolutely NO IgG or IgM antibodies at

> all, meaing the pathogen was definitely in control of the host.

>

> My treatment turned that around. My 2004 test showed a marked

> increase in Lyme antibodies. (2005 test will be back in 2 weeks).

>

> Man. I think they have GOT to figure out some accurate markers of

> how to track whether one is making progress or not. Other wise it

> just seems it's a perpetual guessing game.

>

> Barb

>

>

>

>

>

>

>

>

>

> > >

> > >

> > > > Biofilms, maybe in some cases.

> > >

> > > True.

> > >

> > > > Evolution thru selective pressure in other cases.

> > >

> > > I dont think this is an important factor, at least not on on a

> > month-

> > > to-month scale:

> > >

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

> > >

> > > Antimicrob Agents Chemother. 2005 Apr;49(4):1294-301.

> > >

> > > In vitro susceptibility testing of Borrelia burgdorferi sensu

> lato

> > > isolates cultured from patients with erythema migrans before

and

> > > after antimicrobial chemotherapy.

> > >

> > > Hunfeld KP, Ruzic-Sabljic E, Norris DE, Kraiczy P, Strle F.

> > >

> > > Institute of Medical Microbiology, University Hospital of

> > furt,

> > > -Ehrlich Str. 40, D-60596 furt/Main, Germany.

> > > K.Hunfeld@e...

> > >

> > > Clinical treatment failures have been reported to occur in

early

> > Lyme

> > > borreliosis (LB) for many suitable antimicrobial agents.

> > > Investigations of possible resistance mechanisms of the

Borrelia

> > > burgdorferi complex must analyze clinical isolates obtained

from

> LB

> > > patients, despite their receiving antibiotic treatment. Here,

> > > borrelial isolates obtained from five patients with erythema

> > migrans

> > > (EM) before the start of antibiotic therapy and again after the

> > > conclusion of treatment were investigated. The 10 isolates were

> > > characterized by restriction fragment length polymorphism

> analysis

> > > and plasmid profile analysis and subjected to susceptibility

> > testing

> > > against a variety of antimicrobial agents including those used

> for

> > > initial chemotherapy. Four out of five patients were infected

by

> > the

> > > same genospecies (Borrelia afzelii, n = 3; Borrelia garinii, n

=

> 1)

> > > at the site of the EM lesion before and after antimicrobial

> > therapy.

> > > In one patient the genospecies of the initial isolate (B.

> afzelii)

> > > differed from that of the follow-up isolate (B. garinii). No

> > > significant changes in the in vitro susceptibilities became

> obvious

> > > for corresponding clinical isolates before the start and after

> the

> > > conclusion of antimicrobial therapy. This holds true for the

> > > antimicrobial agents used for specific chemotherapy of the

> > patients,

> > > as well as for any of the additional agents tested in vitro.

Our

> > > study substantiates borrelial persistence in some EM patients

at

> > the

> > > site of the infectious lesion despite antibiotic treatment over

a

> > > reasonable time period. Borrelial persistence, however, was not

> > > caused by increasing MICs or minimal borreliacidal

concentrations

> > in

> > > these isolates. Therefore, resistance mechanisms other than

> > acquired

> > > resistance to antimicrobial agents should be considered in

> patients

> > > with LB resistant to treatment.

> > >

> > > Publication Types:

> > > Clinical Trial

> > >

> > > PMID: 15793100 [PubMed - indexed for MEDLINE]

> > >

> >

>

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