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> ,

> My son did just great on 4 months of some oral form of ceftriaxone,

> but he is not over borrelia. He just takes tons of garlic pills to

> hold his own. I wouldn't be surprised if we just plain have no cure

> for borrelia. But the other half of this problem is that we don't

> have a good way to tell if a person is still actively infected.

>

> I'm not telling anyone anything new here.

>

> a

I'm not convinced it's pathogenic in every, or any, chronic case where

it can be detected. Just for kicks, here's my breakdown:

- Well there's Bowen

- but, Bowen is positive on bloods, which are usually PCR negative

but occasionally PCR positive (Harvey and Salvato, numeric data not

given). This doesn't make much sense, as Barb underlined, and there

seems to be little room for it to be accounted for by various

theoretics. I'm waiting to see if the new lab with the flow cytometer

can get positive PCRs by concentrating the bright bodies.

- Barb's own case is interesting, speaking of Barb, with

seroreversion and partial relpase accompanying sero-reconversion (raw

data not given), at least according to whoever did her WBs ... nothing

against the specialty labs, but they haven't published anything about

why their results differ from standard labs, so I just don't know why

that is.

- Is EM (pathognomonic of acute lyme) associated with later CFS?

Steere says yes. I have JAMA article on file that says no. I haven't

ever read it yet. It may be statistical sophistry.

- Barthold (1994?) found that mice cured of borrelial disease (as far

as he could tell; he can't talk to the mice; but still) still had

borreliae that could be amplified by PCR. They couldn't be transfered

to new mice, ie, they were avirulent; genotypically altered. The

" anti-lyme " point here is that it seemed the mice remained infected,

but they weren't harmed, so you can't draw a firm conclusion from the

simple fact that you harbor borreliae. I don't believe I have read

this paper so I am not 100% confident in what I am saying here. Also,

since borrelia is adapted to infect the mouse (rather benignly) and

probably less adapted to infect the human, the phenomena in the mouse

may be misleading in some ways wrt human health. Anyway, this whole

deal seems to correlate with syphilis. Treponemoid organisms were

observed in treated syphilis patients (I'm not aware that they were

ever nailed down as being Treponema pallidum). Yet the patients don't

relapse progressively, despite the fact that some of them

(neurosyphilis anyway) have residual symptoms that may relate to

residual infection, or may instead represent permanent tissue damage

or postinfectious autoimmunity. The " pro-lyme " point here is that

maybe even " avirulent " organisms that would fail to cause acute

disease when transfered to a new animal, could nevertheless somehow

sustain chronic disease in a host with the proper predispositions.

- I'm sure I had something else to say about this but I can't think

of it. Anyway, I'm not convinced borrelia is important. Needless to

say, I'm also not convinced staph is important (though I would be for

my own case if it were isolated from my bone as in Penny's case,

assuming I didn't think it was a skin contaminant). In short I'm not

convinced of anything. Fortunately for me, I don't have to be

convinced in order to take medical action based on my best guesses.

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On May 26, 2007, at 2:55 PM, wrote:

> I'm not convinced borrelia is important. Needless to

> say, I'm also not convinced staph is important (though I would be for

> my own case if it were isolated from my bone as in Penny's case,

> assuming I didn't think it was a skin contaminant). In short I'm not

> convinced of anything.

I'm not convinced of anything either. My son and I tested positive

for borrelia through IGeneX, but extensive treatment for Lyme didn't

do us much good. I think it helped me a bit in that my digestive

system seems better, so maybe I got rid of some bug there

coincidentally. I thought that abx helped my back pain, but in

retrospect, maybe it was Benicar reducing inflammation while I was on

a certain protocol. It never did get as bad again, but neither did it

continue to get better on heavy duty abx when I switched to

conventional Lyme treatment.

I concluded that since my son and I didn't get a response to Lyme

treatment like Barb's, we likely have a different problem, maybe or

maybe not involving other infections (possibly infection soup). If we

had gone through clear cases of acute Lyme I would still be looking

in that direction, but we didn't.

- Kate

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> - Is EM (pathognomonic of acute lyme) associated with later CFS?

> Steere says yes. I have JAMA article on file that says no. I haven't

> ever read it yet. It may be statistical sophistry.

This is JAMA 283.5.610 if anyone's interested. I have just read parts

of it; don't have time to scrutinize the whole shebang right now. It

does not appear to be total BS. However, ~80% of the patients were

treated at the time of suspicion of acute lyme, so this doesn't

necessarily reflect the natural history of the disease.

There were several outcome measures, yielding a couple of significant

differences (myalgia, p = 0.04, self-reported ability in idea

formulation, p = 0.01) between the lyme history group and the control

group. The discussion invokes the Bonferoni correction for multiple

comparisons, which is hairy territory. Bonferoni aside, judging by the

overall picture of the data, it doesn't look like these people have an

serious excess of CFS.

I don't remember the ref for the Steere statement or what he based it

on. And, he may have referred to some other indication of lyme, not

necessarily EM - I don't recall as precisely as I implied.

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,

I LOVE your last paragraph. Just to add to the confusion here is our

family history.

We all have positive IgG western blots at IgeneX with several bands

positive. We all have positive urine antigen with an antibiotic

challenge. Pete and I used Zithromax, son used ??? I think a

penicillin. We all have positive reverse western blots on those urine

samples.

My husband's symptoms have been SEVERE sciatica and inflammed

prostate - over a period of years. He responds to Zithromax but the

sciatica and muscle pain returns when he discontinues Zithromax. He

is the least symptomatic in general.

My son at age 30 developed a horrible case of rapid

onset " encephalitis " with an MRI indicating brain empty places. (In

spite of which he is a brilliant genius currently traveling in China

on business.) He recovered, but will relapse at times and then

increases his garlic. He claims the brain spaces are from way to much

alcohol - just kidding though - watch out, Tony.

I got cfs, rapid onset, in 1995. I AM THE ONLY ONE WHO HAD A BULL'S

EYE RASH - this fits what you wrote.

Pete and I both have the staph colonization but are resistant to

different antibiotics - weird.

Like you, I will take what works whether I understand it or not, but

I am now careful not to kill myself with dangerous antibiotics such

as quinolones. I was far better off 4 years ago before they

supposedly cured my borrelia and babesia.

a

>

>

> > ,

> > My son did just great on 4 months of some oral form of

ceftriaxone,

> > but he is not over borrelia. He just takes tons of garlic pills

to

> > hold his own. I wouldn't be surprised if we just plain have no

cure

> > for borrelia. But the other half of this problem is that we don't

> > have a good way to tell if a person is still actively infected.

> >

> > I'm not telling anyone anything new here.

> >

> > a

>

>

>

> I'm not convinced it's pathogenic in every, or any, chronic case

where

> it can be detected. Just for kicks, here's my breakdown:

>

> - Well there's Bowen

>

> - but, Bowen is positive on bloods, which are usually PCR negative

> but occasionally PCR positive (Harvey and Salvato, numeric data not

> given). This doesn't make much sense, as Barb underlined, and there

> seems to be little room for it to be accounted for by various

> theoretics. I'm waiting to see if the new lab with the flow

cytometer

> can get positive PCRs by concentrating the bright bodies.

>

> - Barb's own case is interesting, speaking of Barb, with

> seroreversion and partial relpase accompanying sero-reconversion

(raw

> data not given), at least according to whoever did her WBs ...

nothing

> against the specialty labs, but they haven't published anything

about

> why their results differ from standard labs, so I just don't know

why

> that is.

>

> - Is EM (pathognomonic of acute lyme) associated with later CFS?

> Steere says yes. I have JAMA article on file that says no. I haven't

> ever read it yet. It may be statistical sophistry.

>

> - Barthold (1994?) found that mice cured of borrelial disease (as

far

> as he could tell; he can't talk to the mice; but still) still had

> borreliae that could be amplified by PCR. They couldn't be

transfered

> to new mice, ie, they were avirulent; genotypically altered. The

> " anti-lyme " point here is that it seemed the mice remained infected,

> but they weren't harmed, so you can't draw a firm conclusion from

the

> simple fact that you harbor borreliae. I don't believe I have read

> this paper so I am not 100% confident in what I am saying here.

Also,

> since borrelia is adapted to infect the mouse (rather benignly) and

> probably less adapted to infect the human, the phenomena in the

mouse

> may be misleading in some ways wrt human health. Anyway, this whole

> deal seems to correlate with syphilis. Treponemoid organisms were

> observed in treated syphilis patients (I'm not aware that they were

> ever nailed down as being Treponema pallidum). Yet the patients

don't

> relapse progressively, despite the fact that some of them

> (neurosyphilis anyway) have residual symptoms that may relate to

> residual infection, or may instead represent permanent tissue damage

> or postinfectious autoimmunity. The " pro-lyme " point here is that

> maybe even " avirulent " organisms that would fail to cause acute

> disease when transfered to a new animal, could nevertheless somehow

> sustain chronic disease in a host with the proper predispositions.

>

> - I'm sure I had something else to say about this but I can't think

> of it. Anyway, I'm not convinced borrelia is important. Needless to

> say, I'm also not convinced staph is important (though I would be

for

> my own case if it were isolated from my bone as in Penny's case,

> assuming I didn't think it was a skin contaminant). In short I'm not

> convinced of anything. Fortunately for me, I don't have to be

> convinced in order to take medical action based on my best guesses.

>

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Hi Kate,

What if you guys have a primordial soup of infections - typical of

tick bites? I took Zithromax at 500 mg a day for two years and still

relapsed in three months off. I think when they added Mepron to the

Zithro I actually got out of the woods. I've had docs try various

antibiotic combos on me over time. I don't think anything yet has

cured me, but I do feel I am very much better than most (except for

this odd headache now which really doesn't fit where I was for the

past 10 years - feeling a lot better.)Also, Zithromax has worked for

me as a safe maintance antibiotic with no side effects.

I guess I am rambling but trying to suggest maybe you need to just

keep taking some antibiotic to which you ( and son) respond.

a

>

> On May 26, 2007, at 2:55 PM, wrote:

> > I'm not convinced borrelia is important. Needless to

> > say, I'm also not convinced staph is important (though I would be

for

> > my own case if it were isolated from my bone as in Penny's case,

> > assuming I didn't think it was a skin contaminant). In short I'm

not

> > convinced of anything.

>

> I'm not convinced of anything either. My son and I tested positive

> for borrelia through IGeneX, but extensive treatment for Lyme

didn't

> do us much good. I think it helped me a bit in that my digestive

> system seems better, so maybe I got rid of some bug there

> coincidentally. I thought that abx helped my back pain, but in

> retrospect, maybe it was Benicar reducing inflammation while I was

on

> a certain protocol. It never did get as bad again, but neither did

it

> continue to get better on heavy duty abx when I switched to

> conventional Lyme treatment.

>

> I concluded that since my son and I didn't get a response to Lyme

> treatment like Barb's, we likely have a different problem, maybe

or

> maybe not involving other infections (possibly infection soup). If

we

> had gone through clear cases of acute Lyme I would still be

looking

> in that direction, but we didn't.

>

> - Kate

>

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Ksate

there's a tip that occurs when doing cultures bad organisms tend to

dominate spaces..With the highly resistant staph found in the sinus

the other 40 organisms that can be grown have been outcompeted.I

normally get a good garden variety of bacteria and fungii when doing

non sinus disease swabs

> > I'm not convinced borrelia is important. Needless to

> > say, I'm also not convinced staph is important (though I would be

for

> > my own case if it were isolated from my bone as in Penny's case,

> > assuming I didn't think it was a skin contaminant). In short I'm

not

> > convinced of anything.

>

> I'm not convinced of anything either. My son and I tested positive

> for borrelia through IGeneX, but extensive treatment for Lyme

didn't

> do us much good. I think it helped me a bit in that my digestive

> system seems better, so maybe I got rid of some bug there

> coincidentally. I thought that abx helped my back pain, but in

> retrospect, maybe it was Benicar reducing inflammation while I was

on

> a certain protocol. It never did get as bad again, but neither did

it

> continue to get better on heavy duty abx when I switched to

> conventional Lyme treatment.

>

> I concluded that since my son and I didn't get a response to Lyme

> treatment like Barb's, we likely have a different problem, maybe

or

> maybe not involving other infections (possibly infection soup). If

we

> had gone through clear cases of acute Lyme I would still be

looking

> in that direction, but we didn't.

>

> - Kate

>

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If tested, something like 85% of the population would test positive for the herpes virus. Fortunately, nowhere near that many experience outbreaks. I know says the same thing could apply to staph, but it's easy to test whether staph is pathogenic, unlike borrellia. You culture the organisms, then do therapeutic probes with the abx that they test sensitive to. If your symptoms are alleviated to some degree, you know that there's a really good likelihood that the staph (or some other organism) is causing your big problems. Of course not all drugs will maintain their effectiveness. Many are quickly overcome by the organisms' defense mechanisms, but at least you know what you're dealing with. This is what drives me crazy. It's so simple. They do it with my bird. They used to do it right in the doctors' office back in the 40s and 50s. Why can't they do it with

us? Really no reason that I can see, other than economics and fear of what people will do once they wake up to what's going on and the ramifications these infections have for our future. Creating antibiotics is no longer profitable. They can't make them fast enough to keep up with the bugs and still make money. penny pjeanneus <pj7@...> wrote: ,I LOVE your last paragraph. Just to add to the confusion here

is our family history.We all have positive IgG western blots at IgeneX with several bands positive. We all have positive urine antigen with an antibiotic challenge. Pete and I used Zithromax, son used ??? I think a penicillin. We all have positive reverse western blots on those urine samples.My husband's symptoms have been SEVERE sciatica and inflammed prostate - over a period of years. He responds to Zithromax but the sciatica and muscle pain returns when he discontinues Zithromax. He is the least symptomatic in general.My son at age 30 developed a horrible case of rapid onset "encephalitis" with an MRI indicating brain empty places. (In spite of which he is a brilliant genius currently traveling in China on business.) He recovered, but will relapse at times and then increases his garlic. He claims the brain spaces are from way to much alcohol - just kidding though - watch out, Tony. I got

cfs, rapid onset, in 1995. I AM THE ONLY ONE WHO HAD A BULL'S EYE RASH - this fits what you wrote.Pete and I both have the staph colonization but are resistant to different antibiotics - weird. Like you, I will take what works whether I understand it or not, but I am now careful not to kill myself with dangerous antibiotics such as quinolones. I was far better off 4 years ago before they supposedly cured my borrelia and babesia. a>> > > ,> > My son did just great on 4 months of some oral form of ceftriaxone, > > but he is not over borrelia. He just takes tons of garlic pills to > > hold his own. I wouldn't be surprised if we just plain have no cure > > for borrelia. But the other half of this problem is that we don't > > have a good way to tell if a person is still actively infected.> > > > I'm not telling anyone

anything new here.> > > > a> > > > I'm not convinced it's pathogenic in every, or any, chronic case where> it can be detected. Just for kicks, here's my breakdown:> > - Well there's Bowen> > - but, Bowen is positive on bloods, which are usually PCR negative> but occasionally PCR positive (Harvey and Salvato, numeric data not> given). This doesn't make much sense, as Barb underlined, and there> seems to be little room for it to be accounted for by various> theoretics. I'm waiting to see if the new lab with the flow cytometer> can get positive PCRs by concentrating the bright bodies.> > - Barb's own case is interesting, speaking of Barb, with> seroreversion and partial relpase accompanying sero-reconversion (raw> data not given), at least according to whoever did her WBs ... nothing> against the specialty

labs, but they haven't published anything about> why their results differ from standard labs, so I just don't know why> that is.> > - Is EM (pathognomonic of acute lyme) associated with later CFS?> Steere says yes. I have JAMA article on file that says no. I haven't> ever read it yet. It may be statistical sophistry.> > - Barthold (1994?) found that mice cured of borrelial disease (as far> as he could tell; he can't talk to the mice; but still) still had> borreliae that could be amplified by PCR. They couldn't be transfered> to new mice, ie, they were avirulent; genotypically altered. The> "anti-lyme" point here is that it seemed the mice remained infected,> but they weren't harmed, so you can't draw a firm conclusion from the> simple fact that you harbor borreliae. I don't believe I have read> this paper so I am not 100% confident in what I am

saying here. Also,> since borrelia is adapted to infect the mouse (rather benignly) and> probably less adapted to infect the human, the phenomena in the mouse> may be misleading in some ways wrt human health. Anyway, this whole> deal seems to correlate with syphilis. Treponemoid organisms were> observed in treated syphilis patients (I'm not aware that they were> ever nailed down as being Treponema pallidum). Yet the patients don't> relapse progressively, despite the fact that some of them> (neurosyphilis anyway) have residual symptoms that may relate to> residual infection, or may instead represent permanent tissue damage> or postinfectious autoimmunity. The "pro-lyme" point here is that> maybe even "avirulent" organisms that would fail to cause acute> disease when transfered to a new animal, could nevertheless somehow> sustain chronic disease in a host with the proper

predispositions. > > - I'm sure I had something else to say about this but I can't think> of it. Anyway, I'm not convinced borrelia is important. Needless to> say, I'm also not convinced staph is important (though I would be for> my own case if it were isolated from my bone as in Penny's case,> assuming I didn't think it was a skin contaminant). In short I'm not> convinced of anything. Fortunately for me, I don't have to be> convinced in order to take medical action based on my best guesses.>

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>

> If tested, something like 85% of the population would test positive

for the herpes virus. Fortunately, nowhere near that many experience

outbreaks.

Penny,

I may be missing something but Montoya is finding that some cfs

patients have very high IgG titres for EBV and HHV6. CMV doesn't seem

to matter. But the high titres of the first two do seem to relate to

increased symptoms of cfs.

This whole viral thing is new to me, and I wouldn't be looking at it

except that I found a couple of people whose judgement I respect and

who also have Lyme getting treated and responding to antivirals.

So I am thinking that it looks like we add mold toxins, bacteria AND

NOW viruses to the mix.

a

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uh hu

--- pjeanneus <pj7@...> wrote:

>

> >

> > If tested, something like 85% of the population

> would test positive

> for the herpes virus. Fortunately, nowhere near that

> many experience

> outbreaks.

>

> Penny,

> I may be missing something but Montoya is finding

> that some cfs

> patients have very high IgG titres for EBV and HHV6.

> CMV doesn't seem

> to matter. But the high titres of the first two do

> seem to relate to

> increased symptoms of cfs.

>

> This whole viral thing is new to me, and I wouldn't

> be looking at it

> except that I found a couple of people whose

> judgement I respect and

> who also have Lyme getting treated and responding to

> antivirals.

>

> So I am thinking that it looks like we add mold

> toxins, bacteria AND

> NOW viruses to the mix.

>

> a

>

>

>

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On May 26, 2007, at 7:39 PM, pjeanneus wrote:

> Hi Kate,

> What if you guys have a primordial soup of infections - typical of

> tick bites?...

> I guess I am rambling but trying to suggest maybe you need to just

> keep taking some antibiotic to which you ( and son) respond.

It's an idea we can always come back to but I'm not convinced we had

any useful response to any antibiotic we tried. Some did make us feel

somewhat worse but I agree with many on the list that it's not

necessarily " herxing " and it doesn't mean we should keep doing it.

Possibly I killed off something taking a combo of three abx, I might

have felt somewhat better after all that or maybe not. Who knows?

Anyway, it's time for us to look at other factors in our health and

see what we can accomplish there. I do appreciate the freedom to try

abx and I am not taking any " I told you sos " from any docs. Nothing

ventured, nothing gained. Some people DO respond well.

- Kate

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> I know says the same thing could apply to staph, but it's easy

to test whether staph is pathogenic, unlike borrellia. You culture the

organisms, then do therapeutic probes with the abx that they test

sensitive to. If your symptoms are alleviated to some degree, you know

that there's a really good likelihood that the staph (or some other

organism) is causing your big problems.

Well.................. kind of. I see what you're saying, I just

wouldn't go quite as far as the wording " really good likelihood. " The

problem is that the assay isn't specific; it will generate false

positives if you are sickened by borrelia and take something and the

borrelia die. For pretty much any abx you name, either borrelia or Cpn

is naturally sensitive, and like strep and a lot of other bacteria,

they haven't acquired resistances to speak of over the last several

decades the way staph has. So, to my view there's really a lot of

suspect organisms that are likely to get caught in your net.

> Creating antibiotics is no longer profitable. They can't make them

fast enough to keep up with the bugs and still make money.

Yes, the market is a hell of a lot weaker these days, cause it's hard

to come up with something that beats the generics. If you come up with

something comparable to the generics, no one wants it, since the

generics are maybe 3-7x cheaper.

However, there also just aren't that many natural products left that

have awesome antibacterial potential. (Natural products just means

molecules found in nature; most often they come from microbes.) New

antibacterial natural products are often described these days, but

mostly they are just variations on already-known pharmacophores. (The

pharmacophore is the " core " essence of the molecule's structure, like

the four six-membered all-C rings of the tetracyclines, and variants

are minor variations on the pharmacophore, all of which have a similar

biochemical mode of activity.) A new variation of an old pharmacophore

is not totally useless. There will always be some bug somewhere that

can't really be treated with old variants of the pharmacophore, but

can be treated with the new one you just discovered. But still,

cross-resistance to many variants of a given pharmacophore is more the

rule, so what really changes things is *new* pharmacophores.

Some drugs are literally natural products, atom for atom

(streptomycin); just as commonly, though, the natural product is used

in a slightly altered form (eg rifampin) that has better pharmacologic

properties and sometimes better activity.

There are certainly some abx that aren't natural products. But most

people seem to think natural products are still the richest sources

for drug discovery of most kinds, including antimicrobial discovery.

Maybe one day, computational drug discovery will revolutionize

non-natural drug discovery. But there seems to be no strong indication

right now that that will necessarily ever happen.

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,

This leads me to ask what about phages? Any thoughts?

a Carnes

> However, there also just aren't that many natural products left that

> have awesome antibacterial potential. (Natural products just means

> molecules found in nature; most often they come from microbes.) New

> antibacterial natural products are often described these days, but

> mostly they are just variations on already-known pharmacophores.

(The

> pharmacophore is the " core " essence of the molecule's structure,

like

> the four six-membered all-C rings of the tetracyclines, and variants

> are minor variations on the pharmacophore, all of which have a

similar

> biochemical mode of activity.) A new variation of an old

pharmacophore

> is not totally useless. There will always be some bug somewhere that

> can't really be treated with old variants of the pharmacophore, but

> can be treated with the new one you just discovered. But still,

> cross-resistance to many variants of a given pharmacophore is more

the

> rule, so what really changes things is *new* pharmacophores.

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, I'm just using staph as an example of a tough bug, but if you identify any organism and take the drugs it tests sensitive to and you have a favorable response, how can you say that there's not a really good likelihood that you've got a bacterial problem? Who cares if other bugs are getting killed in the process? All the better. I'm using staph as a good candidate for serious investigation because we know it's common, deadly, and extremely resistant to treatment AND that it overpowers a lot of other bugs (with it's own anti-microbial toxins). So if you can impact staph with a drug, then you've got a good chance of killing whatever else might be involved in making you sick. If by chance, one of those secondary bugs is actually resistant to the drug the staph is sensitive to, then you could suddenly develop symptoms of that other bug's opportunistic explosive growth caused by the

die-off of the staph, which could be one explanation for the need of multiple abx therapies (and the famous so-called "herx" when you suddenly get ill due to the secondary bug getting stronger). This is why it's so important to identify all the bugs you're carrying and test them for drug sensitivities and treat accordingly. In my view, Abx guesswork is close to idiotic when dealing with the resistant bugs we're dealing with and should only be used as a last resort. Unfortunately, the majority of doctors and labs ignore staph, which is really stupid in my book, so we do end up having to use educated guesswork to some degree (unfortunately). If you do get tests that show resistant bugs and take the drugs your bugs are still sensitive to, and see no results at all (which I haven't actually seen happen in anyone) then it's pretty likely that you

should be looking at another source for your illness. To me it would just make everything so much simpler if people could just get tested, give the corresponding therapy a shot and see what happens. Everyone I know who's done that has improved considerably. Usually it is a combo of bugs that are contributing to your illness. But knocking down the most resilient of them seems to have the biggest impact on your health. At least it did for me. I tested positive for several bugs. Prior to antibiotics, I could barely think straight or sit upright at the computer without feeling like I might fall off my chair. I'm not 100% yet, and that's because I have to get to the source of my infection in the bone. According to the standard treatment for osteomyelitis, that's done with debridement, which is pretty scary. But just by using the correct abx treatment alone, I'm way better than I have been with

any other therapy I tried prior to (or since) identifying and treating my organisms correctly. This is what everyone I know who has identified their chronic bugs is doing, and all of us feel it's the only thing that's really saving us. It's certainly not an unusual concept to the infectious disease docs we are working with, but to the general pwc community it's about as alien as the X-files. penny <usenethod@...> wrote: > I know says the same thing could apply to staph, but it's easyto test whether staph is pathogenic, unlike borrellia. You culture theorganisms, then do therapeutic probes with the abx that they testsensitive to. If your symptoms are alleviated to some degree, you knowthat there's a really good likelihood that the staph (or some otherorganism) is causing your big problems. Well.................. kind of. I see what you're saying, I justwouldn't go quite as far as the wording "really good likelihood." Theproblem is that the assay isn't specific; it will generate falsepositives if you are sickened by borrelia and take something and theborrelia die. For pretty much any abx you name, either borrelia or Cpnis naturally sensitive, and like strep and a lot of other bacteria,they haven't acquired resistances to speak of over the last severaldecades the way staph has. So, to my view there's really a

lot ofsuspect organisms that are likely to get caught in your net. > Creating antibiotics is no longer profitable. They can't make themfast enough to keep up with the bugs and still make money.Yes, the market is a hell of a lot weaker these days, cause it's hardto come up with something that beats the generics. If you come up withsomething comparable to the generics, no one wants it, since thegenerics are maybe 3-7x cheaper.However, there also just aren't that many natural products left thathave awesome antibacterial potential. (Natural products just meansmolecules found in nature; most often they come from microbes.) Newantibacterial natural products are often described these days, butmostly they are just variations on already-known pharmacophores. (Thepharmacophore is the "core" essence of the molecule's structure, likethe four six-membered all-C rings of the tetracyclines, and variantsare minor

variations on the pharmacophore, all of which have a similarbiochemical mode of activity.) A new variation of an old pharmacophoreis not totally useless. There will always be some bug somewhere thatcan't really be treated with old variants of the pharmacophore, butcan be treated with the new one you just discovered. But still,cross-resistance to many variants of a given pharmacophore is more therule, so what really changes things is *new* pharmacophores.Some drugs are literally natural products, atom for atom(streptomycin); just as commonly, though, the natural product is usedin a slightly altered form (eg rifampin) that has better pharmacologicproperties and sometimes better activity.There are certainly some abx that aren't natural products. But mostpeople seem to think natural products are still the richest sourcesfor drug discovery of most kinds, including antimicrobial discovery.Maybe one day,

computational drug discovery will revolutionizenon-natural drug discovery. But there seems to be no strong indicationright now that that will necessarily ever happen.

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> I just came across one interesting lead on

> borrelia being intracellular - never mind the L forms and cyst forms

Love to see it, if you have a new ref on this. I'll probably be going

to the National Library of Medicine tomorrow morning.

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, I send the article and comments off list to you, as I don't have

permission to post it here. Of course, if you can find the article at

the library I would be most interested to read your insights.

a Carnes

>

> > I just came across one interesting lead on

> > borrelia being intracellular - never mind the L forms and cyst

forms

>

> Love to see it, if you have a new ref on this. I'll probably be going

> to the National Library of Medicine tomorrow morning.

>

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