Re: antibiotic therapy reducing gut microflora

[Guest guest]

Nelly,

I am so sorry to hear about the horrifying three days. When I hear

that from you I cringe because I know you are a seasoned veteran.

I don't know what to make of Donta's take on this. He is saying

there are metabolic products, which are perfectly normal, coming

from normal gut flora, and normally they do not bother the brain but

our brains they do bother. Is that right?

I've been encouraged by some of your recent posts, though I know you

are cautious about optimistic predictions. In any case, I think of

you often and always with great fondness.

Your brain-challenged friend,

> This is Sam Donta's opinion re why abx (metronidazole for eg) work

transiently by reducing the gut flora and therefore the metabolic

products which participate in the neuro probs we (Lyme patients)

experience.

>

> http://www.lymediseaseaction.org.uk/conference/prog04.htm

>

> Can someone comment as to why Donta seems to be so adamant that Bb

are not affected by imidazoles (and I suppose Chlam.pneum)? Does

anybody know why Donta chooses to completely ignore the

cystic/cryptic forms of the bacterias?

>

> Nelly (just had the most horrifying 3 days after 3 days of

tinidazole as my second stint with it as per Wheldon/Stratton, yet I

have already taken loads of tinidazole)

>

> Now, there is an interesting thing here and this raises a big

question about what it is that we do with treatment. And it is a

little bit of a digression but I think perhaps it is an important

one. Metronidazole, Flagyl, as it is called in the United States,

has been used in Lyme Disease based on the idea that it might affect

the cyst form but when you look at the genome of the Borrelia they

do not contain any sequences to metabolise Metronidazole so there is

no way the Metronidazole can have a direct effect on the Borrelia.

So, how is it that clinically some patients who are on this seem to

have a transient response?

>

> I have thought about this for a while and it takes me about 4 or 5

years to figure things out but whether I have figured it out or not

but what I think may be happening and here is the analogy: When you

have a patient who has cirrhosis of the liver from either alcoholism

or from Hepatitis, one of the things that they do is to go into a

coma or not necessarily a coma but confusional state and that is

thought to be due to the absorption of some metabolic products of

the intestinal bacteria.

>

> So what do we do in that case, we give them Neomycin, an

antibiotic which just stays in the intestine, and it reduces the

amount of the intestinal flora and thereby decreasing the metabolic

products which have to be detoxified by the liver and in that case

the liver is impaired. Well how do I jump from that to the Lyme

patient and Metronidazole and let me put Cholestyramine in the

picture too and perhaps any antibiotic, scary as that may be. What

if we are, in the Lyme patient, that in the non- Lyme patient the

metabolic products don't make any difference. Not as far as we know.

This is our brain, this is our state of confusion, our state of

memory.

>

> What if the Lyme patient is sensitised because we know the Lyme

patient is sensitised to wherever their focus is they are sensitised

to stimuli, they may be de-sensitised too, but what if some of the

metabolic products with an intact liver are creating a problem with

the sensitivity of the neurons and maybe what we are doing with the

Metronidazole or Cholestyramine in the case of binding metabolic

products and temporarily making a person feel better. What if some

of our antibiotic therapy is reducing some of the other microflora

and we are transiently then reducing some other. In other words,

what if this is a secondary effect. How do we know that it is a

direct effect on it.

[Guest guest]

Thanks for posting that, most interesting. I am very surprised he

would say that stuff without addressing the Brorson in vitro

observations.

<janel@p...> wrote:

> This is Sam Donta's opinion

[Guest guest]

,

Yes, that's one of the things that surprised me too, yet I know that the Brorson's study doesn't seem to be taken very seriously outside of LLMDs, other ID doctors never appear to include that cystic Bb form into their thinking of chronic Lyme.

My ID doctor (Lyme friendly) agreed to Rx tinidazole for me and he did try it with other Lyme patients a few years ago with very spectacular initial results, but when the patients "hit the tini/metronidazole wall" after a few days or a few weeks, I think he chickened out and he does not Rx it now (except to me, as I keep coming up with good reasons why he should).

I have now given him the Wheldon/Stratton article that says that metronidazole is needed to fight chronic chlam.pneu.

Nelly

[infections] Re: antibiotic therapy reducing gut microflora

Thanks for posting that, most interesting. I am very surprised hewould say that stuff without addressing the Brorson in vitroobservations. <janel@p...> wrote:> This is Sam Donta's opinion

[Guest guest]

On Sunday, May 1, 2005, at 05:39 PM, Nelly Pointis wrote:

> Does anybody know why Donta chooses to completely ignore the

> cystic/cryptic forms of the bacterias?

In that same talk, he made some comment about dead bacteria curling up

inside cells, and you could call them cysts if you want....

- Kate D.

[Guest guest]

Nelly wrote (quoting Donta):

" What if some

of our antibiotic therapy is reducing some of the other microflora

and we are transiently then reducing some other. In other words,

what if this is a secondary effect. How do we know that it is a

direct effect on it. "

Nelly:

Yes, I think that could be a possibility (and why some people

relapse after ceasing abx).

The other thing to remember, is that some species in the gut

(intestine) actually GROW in the presence of certain abx, and their

population reduces when the abx is withdrawn. This would be another

reason people can feel progressively worse on abx.

What happened with you and Tini?

Barb

> > This is Sam Donta's opinion re why abx (metronidazole for eg)

work

> transiently by reducing the gut flora and therefore the metabolic

> products which participate in the neuro probs we (Lyme patients)

> experience.

> >

> > http://www.lymediseaseaction.org.uk/conference/prog04.htm

> >

> > Can someone comment as to why Donta seems to be so adamant that

Bb

> are not affected by imidazoles (and I suppose Chlam.pneum)? Does

> anybody know why Donta chooses to completely ignore the

> cystic/cryptic forms of the bacterias?

> >

> > Nelly (just had the most horrifying 3 days after 3 days of

> tinidazole as my second stint with it as per Wheldon/Stratton, yet

I

> have already taken loads of tinidazole)

> >

> > Now, there is an interesting thing here and this raises a big

> question about what it is that we do with treatment. And it is a

> little bit of a digression but I think perhaps it is an important

> one. Metronidazole, Flagyl, as it is called in the United States,

> has been used in Lyme Disease based on the idea that it might

affect

> the cyst form but when you look at the genome of the Borrelia they

> do not contain any sequences to metabolise Metronidazole so there

is

> no way the Metronidazole can have a direct effect on the Borrelia.

> So, how is it that clinically some patients who are on this seem to

> have a transient response?

> >

> > I have thought about this for a while and it takes me about 4 or

5

> years to figure things out but whether I have figured it out or not

> but what I think may be happening and here is the analogy: When you

> have a patient who has cirrhosis of the liver from either

alcoholism

> or from Hepatitis, one of the things that they do is to go into a

> coma or not necessarily a coma but confusional state and that is

> thought to be due to the absorption of some metabolic products of

> the intestinal bacteria.

> >

> > So what do we do in that case, we give them Neomycin, an

> antibiotic which just stays in the intestine, and it reduces the

> amount of the intestinal flora and thereby decreasing the metabolic

> products which have to be detoxified by the liver and in that case

> the liver is impaired. Well how do I jump from that to the Lyme

> patient and Metronidazole and let me put Cholestyramine in the

> picture too and perhaps any antibiotic, scary as that may be. What

> if we are, in the Lyme patient, that in the non- Lyme patient the

> metabolic products don't make any difference. Not as far as we

know.

> This is our brain, this is our state of confusion, our state of

> memory.

> >

> > What if the Lyme patient is sensitised because we know the Lyme

> patient is sensitised to wherever their focus is they are

sensitised

> to stimuli, they may be de-sensitised too, but what if some of the

> metabolic products with an intact liver are creating a problem with

> the sensitivity of the neurons and maybe what we are doing with the

> Metronidazole or Cholestyramine in the case of binding metabolic

> products and temporarily making a person feel better. What if some

> of our antibiotic therapy is reducing some of the other microflora

> and we are transiently then reducing some other. In other words,

> what if this is a secondary effect. How do we know that it is a

> direct effect on it.

[Guest guest]

Possibly his use of the word variant includes the cyst form.

I have seen the terms Cyst, L form, S form all used interchangable.

Barb

>

> > Does anybody know why Donta chooses to completely ignore the

> > cystic/cryptic forms of the bacterias?

>

> In that same talk, he made some comment about dead bacteria curling

up

> inside cells, and you could call them cysts if you want....

>

> - Kate D.

[Guest guest]

Barb, you've been looking at this literature a lot longer than I

have. Do you feel some confidence that the nomenclature corresponds

to well-defined entities?

In other words, do you feel that we " know " what these words

describe, or even that they are descriptive of reality?

I find it so crazy-making when what I think of as " the basics " are

poorly understood, and here we are wondering if someone who treats

Lyme patients, whose views are taken seriously by Lyme

patients, " believes " in cysts.

I've seen clear, consistent images of spirochetes from microscopy. I

have never seen clear, consistent images of " blebs, " nor would I

know what to look for to distinguish them from any other tiny speck

of organic matter. Would that change, if I read all the research?

> >

> > > Does anybody know why Donta chooses to completely ignore the

> > > cystic/cryptic forms of the bacterias?

> >

> > In that same talk, he made some comment about dead bacteria

curling

> up

> > inside cells, and you could call them cysts if you want....

> >

> > - Kate D.

[Guest guest]

We as lay people have to be carefull that we interpret what

professionals are saying correctly. Those in any business have terms

that are understood within the business, and not understood

by people outside that expertise.

Donta is an Infectious Disease expert, so of course he understands

the variant form(s). This includes the Lyme variant.

He reveals that he's reading the antimicrobial chemotherapy research

literature in regards to different classes of abx promoting varaints

(and in some cases more than one form). And he credits the French

researcher with the original idea of alkalizing the cell compartment

to make macrolides more intracellularily effective.

I think what he's questioning, by politely not being pointed about

it,

is the question of whether only certain chemical classes are

effective on the (Lyme) variant.

Barb

> > >

> > > > Does anybody know why Donta chooses to completely ignore the

> > > > cystic/cryptic forms of the bacterias?

> > >

> > > In that same talk, he made some comment about dead bacteria

> curling

> > up

> > > inside cells, and you could call them cysts if you want....

> > >

> > > - Kate D.

[Guest guest]

I'm not as polite as Donta, so I'll repeat my question: in your

opinion, does medical science " know " what cysts are, how they relate

to sickness or recovery?

I've seen studies discussing in a very matter of fact way that

cystic forms of borrelia survive antibiotic treatment. What I am

unsure of is whether in describing these residual organisms the

researchers are employing some clear and agreed upon understanding

of what the " cyst form " represents.

I have seen studies which look more directly at what they

call " blebs, " and describe pinched off pieces of larger organisms

which either do or do not appear to function as eggs and " hatch " the

larger organism from which they came. In some of his papers on Lyme

arthritis Steere makes it clear he does not view these " blebs " as

part of the borrelia reproduction cycle. At least, that is how I

read his papers on the subject. Perhaps it corresponds in some way

to his notions about how Lyme should be simple to treat?

Pinching off a part of yourself and turning yourself into some

completely different form are not comparable acts. How can the nouns

that correspond to these verbs - " blebs " and " cysts " be

interchangeable?

I don't get it.

> > > >

> > > > > Does anybody know why Donta chooses to completely ignore

the

> > > > > cystic/cryptic forms of the bacterias?

> > > >

> > > > In that same talk, he made some comment about dead bacteria

> > curling

> > > up

> > > > inside cells, and you could call them cysts if you want....

> > > >

> > > > - Kate D.

[Guest guest]

PAUL ASKS:

> I'm not as polite as Donta, so I'll repeat my question: in your

> opinion, does medical science " know " what cysts are, how they

relate

> to sickness or recovery?

BARB REPLIES:

From reading the literature, I think:

They know cysts are a variant form, they know that samll spirochete

(or multiple chetes) can emerge from within a cyst (which is very

interesting), they know the cyst form has additional/different cell

wall proteins from the parent form and is many layered, and they

know know the cyst form is a sucessfull survival mechanism -

but no, they do not know how cysts relate to sickness or recovery in

regards to say... which is worse symptomactically - a colony of

classical spirochetes - or a gaggle of cysts.. not that I've read

anywhere anyway.

PAUL ASKS:

>

> I've seen studies discussing in a very matter of fact way that

> cystic forms of borrelia survive antibiotic treatment. What I am

> unsure of is whether in describing these residual organisms the

> researchers are employing some clear and agreed upon understanding

> of what the " cyst form " represents.

BARB REPLIES:

Sort of the same question.

In terms of survival of the organism, in protein make up, yes.

In contribution to disease symptoms, no.

> PAUL ASKS:

> I have seen studies which look more directly at what they

> call " blebs, " and describe pinched off pieces of larger organisms

> which either do or do not appear to function as eggs and " hatch "

the

> larger organism from which they came. In some of his papers on Lyme

> arthritis Steere makes it clear he does not view these " blebs " as

> part of the borrelia reproduction cycle. At least, that is how I

> read his papers on the subject. Perhaps it corresponds in some way

> to his notions about how Lyme should be simple to treat?

BARB REPLIES:

No- blebbing is not part of a replication cycle.

Many bactera bleb - sometimes it's during the death act or during

what called starvation mode. Researchers do not know for sure when Bb

forms blebs, and sheds some of it's DNA if it's doing so during death

of the organism, or wheher it's part of a (sucessfull) survival

mechanism.. or both.

PAUL ASKS:

>

> Pinching off a part of yourself and turning yourself into some

> completely different form are not comparable acts. How can the

nouns

> that correspond to these verbs - " blebs " and " cysts " be

> interchangeable?

BARB REPLIES:

During the morphing process, there are proteins and enzymes formed

by the bacteria to accomplish this transformation. Blebs can be formed

during the transition to a cyst.

Blebbing is not a completely understood (bacterial) mechanism..

>PAULS SAYS:

> I don't get it.

>

BARB REPLIES:

Don't worry- you're in good company.

Barb

>

>

>

> > > > >

> > > > > > Does anybody know why Donta chooses to completely ignore

> the

> > > > > > cystic/cryptic forms of the bacterias?

> > > > >

> > > > > In that same talk, he made some comment about dead bacteria

> > > curling

> > > > up

> > > > > inside cells, and you could call them cysts if you want....

> > > > >

> > > > > - Kate D.

[Guest guest]

[infections] Re: antibiotic therapy reducing gut microflora

PAUL ASKS:> I'm not as polite as Donta, so I'll repeat my question: in your > opinion, does medical science "know" what cysts are, how they relate > to sickness or recovery?BARB REPLIES:From reading the literature, I think:They know cysts are a variant form, they know that samll spirochete (or multiple chetes) can emerge from within a cyst (which is very interesting), they know the cyst form has additional/different cell wall proteins from the parent form and is many layered, and they know know the cyst form is a sucessfull survival mechanism - but no, they do not know how cysts relate to sickness or recovery in regards to say... which is worse symptomactically - a colony of classical spirochetes - or a gaggle of cysts.. not that I've read anywhere anyway.PAUL ASKS:> > I've seen studies discussing in a very matter of fact way that > cystic forms of borrelia survive antibiotic treatment. What I am > unsure of is whether in describing these residual organisms the > researchers are employing some clear and agreed upon understanding > of what the "cyst form" represents.BARB REPLIES:Sort of the same question.In terms of survival of the organism, in protein make up, yes.In contribution to disease symptoms, no.

NELLY says:

I think I did read that "Bb cysts" did cause inflammation by triggering the production of pro-inflammatory cytokines (don't quote me, I feel too tired to look anything up). In the Polish study below I am not sure whether they make the distinction btwn sxs caused by Bb in spiro form and Bb in cystic, bleb-format but I have read some place that blebs (if not cysts) cause irritation of something or other

Nelly (struggling)

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=12194230

Przegl Epidemiol. 2002;56 Suppl 1:57-67.

Related Articles,

Links

[New aspects of the pathogenesis of lyme disease][Article in Polish]Zajkowska JM, Hermanowska-Szpakowicz T.Klinika Chorob Zakaznych i Neuroinfekcji AM w Bialymstoku.Morphological changes of B. burgdorferi as well as changes in expression of surface proteins caused by environmental determinants are essential in pathogenesis of Lyme disease. Cysts, spherical form (spheroplasts, L-form) and "blebs" (gemmae) can be responsible for long lasting antigenic stimulation, signs of chronic borreliosis, and even probably connected with MS and Alzheimer disease. Mechanisms to avoid elimination and persistence in the host include: expression of low heterogenic Osp A, B replaced by polymorphic in sequence and antigenic reactivity OspC, the hindrance of access to some membrane proteins by other proteins on the spirochete's surface, effects of tick saliva proteins action. Hiding of spirochetes is possible by invagination into fibrocytes membrane as well as, coating by antigens derived from lymphocytes B. Distribution of spirochetes is facilitated by binding to platelets through integrin aIIb b3, and to the endothelial cells through integrins av b3 i a5b1, recognition of decorin by lipoproteins DbpA i DbpB, receptor for NAG (N-acetyl glucosamina). Endothelial cells, toxic products of granulocytes, monocytes, macrophages as well as phagocytosis counterpart in pathogenesis. Induced cytokines are connected with activation subsets of T lymphocytes involved in inflammatory response. Cytokines produced by Th1 as cytotoxic CD8 accompany the disease. Important are also dendritic cells regarded as initiators of Th1 response with participation of IL-12. In pathogenesis of Lyme disease participation of autoimmunity is notified, especially molecular similarities between OspA and human lymphocytic antigen (hLFA-1). Neurotoxin, produced by B. burgdorferi Bbtox1 was identified. Encephalopathy signs in Lyme borreliosis could be result of releasing toxico-metabolic products, ability of spirochetes to pass the blood-brain barrier as well as, effect of lymphocytes migration. Active invasion of brain endothelium as ability to adherence to endothelial wall could be the source of focused or disseminated inflammation of brain vessels. Antiaxonal antibodies could disturb axon conduction without damaging. But damage of white matter could be connected with damage of mielin production cells, probably by antibodies, induced in cross reaction.Publication Types:

Review Review, Tutorial PMID: 12194230 [PubMed - indexed for MEDLINE]

[Guest guest]

sir, like you I am not too wild about the precision of works

addressing pleomorphism.

Classical-morph spirochetes can form large bodies of a diameter

several times that of the spirochete proper. These are most comonly

formed at one end. I'm pretty sure its determined that they can

detatch and progeny form within them. So this is something short of

enclosed encytment of the entire organism.

You might want to look at some mid-20th-century works like these, or

other stuff in the same series, or by the same authors. I have these

but havnet combed em yet. I think (not sure) all this can be accessed

online at the Journal of Bacteriology:

Hampp EC et al morph. charect. of certain cultured strains of oral

spir. and trep pall as revealed by the E.M. J BACTERIOL 56:755-69 1948

Bladen HA Hampp EG ultrastruct of trep pall and borrelia vincentii J

BACTERIOL 87:1180-1191, 1964.

> I'm not as polite as Donta, so I'll repeat my question: in your

> opinion, does medical science " know " what cysts are, how they relate

> to sickness or recovery?

>

> I've seen studies discussing in a very matter of fact way that

> cystic forms of borrelia survive antibiotic treatment. What I am

> unsure of is whether in describing these residual organisms the

> researchers are employing some clear and agreed upon understanding

> of what the " cyst form " represents.

>

> I have seen studies which look more directly at what they

> call " blebs, " and describe pinched off pieces of larger organisms

> which either do or do not appear to function as eggs and " hatch " the

> larger organism from which they came. In some of his papers on Lyme

> arthritis Steere makes it clear he does not view these " blebs " as

> part of the borrelia reproduction cycle. At least, that is how I

> read his papers on the subject. Perhaps it corresponds in some way

> to his notions about how Lyme should be simple to treat?

>

> Pinching off a part of yourself and turning yourself into some

> completely different form are not comparable acts. How can the nouns

> that correspond to these verbs - " blebs " and " cysts " be

> interchangeable?

>

> I don't get it.

>

>

>

[Guest guest]

http://www.lymeinfo.net/medical/LDAdverseConditions.pdf

Everybody has seen this but if you want to have a good look at cysts, blebs etc from research dating very far back for some of it

Nelly

[infections] Re: antibiotic therapy reducing gut microflora

sir, like you I am not too wild about the precision of worksaddressing pleomorphism.Classical-morph spirochetes can form large bodies of a diameterseveral times that of the spirochete proper. These are most comonlyformed at one end. I'm pretty sure its determined that they candetatch and progeny form within them. So this is something short ofenclosed encytment of the entire organism.You might want to look at some mid-20th-century works like these, orother stuff in the same series, or by the same authors. I have thesebut havnet combed em yet. I think (not sure) all this can be accessedonline at the Journal of Bacteriology:

[Guest guest]

Nelly-

Yes- I think Donta said everyone has to be carefull theory doesn't

morph into dogma.

The thing is- wouldn't you think that I of all people would have

been loaded with the cyst form - and probably had a bazillion

colonies of tangles siprochetes in other tissues?

How come I'm symptoms free without taking a macrolide? (I made it 3

days on Zith (in combo with 2 others) and my bilirubin shot up - so

no more Zith for me (and this was well into therapy).

I have to think that it was the ton of HCQ (hydroxychloroquine) I

took with Doxy and Mino.. and I know my tissues were still saturated

when it when I was on Augmentin, and Amoxy.

I've avoided Flagyl and Cipro for admittedly biased & non-rational

scary reasons.

Maybe it is true that Lauricidin (monolaurin) and virgin Coconut oil

can damage the lipid membrane of the Lyme variant.. I don't have the

answers for why I was such a positive responder - but I don't know

too many others that took the doses of HCQ and lauricidin mixed with

their abx that I did.

I really really wish the medical establishement would take this all

seriously enough to get to the real truth so we weren't all just

bumping along in the dark.

Barb

> http://www.lymeinfo.net/medical/LDAdverseConditions.pdf

>

> Everybody has seen this but if you want to have a good look at

cysts, blebs etc from research dating very far back for some of it

>

> Nelly

> [infections] Re: antibiotic therapy

reducing gut microflora

>

>

> sir, like you I am not too wild about the precision of works

> addressing pleomorphism.

>

> Classical-morph spirochetes can form large bodies of a diameter

> several times that of the spirochete proper. These are most

comonly

> formed at one end. I'm pretty sure its determined that they can

> detatch and progeny form within them. So this is something short

of

> enclosed encytment of the entire organism.

>

> You might want to look at some mid-20th-century works like these,

or

> other stuff in the same series, or by the same authors. I have

these

> but havnet combed em yet. I think (not sure) all this can be

accessed

> online at the Journal of Bacteriology:

[Guest guest]

Barb,

You asked me what happened with the tini, here goes:

Since feb 23rd:

doxy 200 mg and a macrolide (spiramycine) for 4 weeks

week 1-2-3 very tired but much improved sleep (getting to sleep easily and waking up early almost refreshed), end of week 3 feeling unbelievably depressed with uncontrolable crying spells starting 4pm lasting 3 or 4 hours for about a week. It was so bad I postponed taking the tini until I the crying had stopped (I was also on my own for a couple of weeks and didn't want to start the tinidazole whilst on my own)

week 4, tinidazole for 5 days (I suspended the doxy and macrolide whilst taking the tini) sore eyes (maybe a bit worse than usual)

week 5 back on doxy and macrolide: very sore right hip, knee, all right side painful, bout of diarrhea, eyes very sore (eyeball pain as well)

week 6 extreme headache (inflamed meninges?) and eyeache

week 7 OKish

week 8 suspended doxy and macrolide and took 3 days of tinidazole and came down with something that could be described as a fainting spell, heart beating very shallowly, feeling very weak, nauseous, had to lie down in my car feet up on the seat head down on the steeering wheel as low as I could get it, drove home like a zombie thinking I would never make it back alive. I had been on one of my very rare outings, out for lunch with friends, (one of them a neurologist about 50 medline refs to her name and she was totally useless, staring at me like I was a freak, but that's another story, I am soon going to sound like Scha on one of his purple days!)

HEADACHE, EYES extremely sore, VERTIGO, nauseous, spent two whole days in bed in the dark, taking every NSAIDS, codeine, aspirin, clonazepam (rivotril) etc in an attempt to knock myself out (I would've gladly died). I had stopped all abx

week 9

back on doxy + macrolide + artemisinin, not as bad as last week but head feeling very inflamed and eyes sore

Nelly (BTW: I think I am the coiner of the expression "flagyl wall")

PS eyes too sore not reading over so excuse spelling etc

[infections] Re: antibiotic therapy reducing gut microflora

Nelly wrote (quoting Donta):"What if someof our antibiotic therapy is reducing some of the other microfloraand we are transiently then reducing some other. In other words,what if this is a secondary effect. How do we know that it is adirect effect on it."Nelly: Yes, I think that could be a possibility (and why some people relapse after ceasing abx). The other thing to remember, is that some species in the gut (intestine) actually GROW in the presence of certain abx, and their population reduces when the abx is withdrawn. This would be another reason people can feel progressively worse on abx.What happened with you and Tini?Barb

[Guest guest]

> Nelly B12 and the rest have been really useful with these symptoms for

> me.

>

> HEADACHE, EYES extremely sore, VERTIGO, nauseous, spent two whole days

> in bed in the dark, taking every NSAIDS, codeine, aspirin, clonazepam

> (rivotril) etc in an attempt to knock myself out (I would've gladly

> died). I had stopped all abx

> Barb,

>  

> You asked me what happened with the tini, here goes:

>  

> Since feb 23rd:

>  

>  doxy 200 mg and a macrolide (spiramycine) for 4 weeks

>  

>  week 1-2-3 very tired but much improved sleep (getting to sleep

> easily and waking up early almost refreshed), end of week 3 feeling

> unbelievably depressed with uncontrolable crying spells starting 4pm

> lasting 3 or 4 hours for about a week. It was so bad I postponed

> taking the tini until I the crying had stopped (I was also on my own

> for a couple of weeks and didn't want to start the tinidazole whilst

> on my own)

>  

> week 4, tinidazole for 5 days (I suspended the doxy and macrolide

> whilst taking the tini) sore eyes (maybe a bit worse than usual)

>  

> week 5 back on doxy and macrolide: very sore right hip, knee, all

> right side painful, bout of diarrhea, eyes very sore (eyeball pain as

> well) 

>  

> week 6 extreme headache (inflamed meninges?) and eyeache

>  

> week 7 OKish

>  

> week 8 suspended doxy and macrolide and took 3 days of tinidazole and

> came down with something that could be described as a fainting spell,

> heart beating very shallowly, feeling very weak, nauseous, had to lie

> down in my car feet up on the seat head down on the steeering wheel as

> low as I could get it, drove home like a zombie thinking I would never

> make it back alive. I had been on one of my very rare outings, out for

> lunch with friends, (one of them a neurologist about 50 medline refs

> to her name and she was totally useless, staring at me like I was a

> freak, but that's another story, I am soon going to sound like

> Scha on one of his purple days!)

>  

> HEADACHE, EYES extremely sore, VERTIGO, nauseous, spent two whole days

> in bed in the dark, taking every NSAIDS, codeine, aspirin, clonazepam

> (rivotril) etc in an attempt to knock myself out (I would've gladly

> died). I had stopped all abx

>  

>  

> week 9

>  

> back on doxy + macrolide + artemisinin, not as bad as last week but

> head feeling very inflamed and eyes sore

>  

> Nelly (BTW: I think I am the coiner of the expression " flagyl wall " )

>  

> PS eyes too sore not reading over so excuse spelling etc

>  

>  

>> [infections] Re: antibiotic therapy reducing

>> gut microflora

>>

>> Nelly wrote (quoting Donta):

>> " What if some

>> of our antibiotic therapy is reducing some of the other microflora

>> and we are transiently then reducing some other. In other words,

>> what if this is a secondary effect. How do we know that it is a

>> direct effect on it. "

>>

>>

>> Nelly:

>>

>>  Yes, I think that could be a possibility (and why some people

>> relapse after ceasing abx).

>>  

>>  The other thing to remember, is that some species in the gut

>> (intestine) actually GROW in the presence of certain abx, and their

>> population reduces when the abx is withdrawn. This would be another

>> reason people can feel progressively worse on abx.

>>

>> What happened with you and Tini?

>>

>> Barb

>>

>

>

[Guest guest]

Bleu,

I take 10 000 mcg sublingual per day, doesn't help one bit (not that I can tell anyway)

Nelly

[infections] Re: antibiotic therapy reducing gut microfloraNelly wrote (quoting Donta):"What if someof our antibiotic therapy is reducing some of the other microfloraand we are transiently then reducing some other. In other words,what if this is a secondary effect. How do we know that it is adirect effect on it."Nelly: Yes, I think that could be a possibility (and why some people relapse after ceasing abx). The other thing to remember, is that some species in the gut (intestine) actually GROW in the presence of certain abx, and their population reduces when the abx is withdrawn. This would be another reason people can feel progressively worse on abx.What happened with you and Tini?Barb