yguner's Antibiotics Log

A forum for the discussion of antibiotics as a potential therapy for MS

Postby yguner » Fri May 13, 2005 4:29 am

I am a progressive MS patient from Istanbul – Turkey and diagnosed 13 years ago with progressive ms. Now my EDSS disability score is 8,5. I started using antibiotics after I read about dr.srirams patented invention and decided to start the antibiotics treatment 9 months ago. I started taking MINOCYLINE 100 mg. X 2 a day and RIFADIN 300 mg. X 2 day for the first six months and switched to antibiotic combination INH 300 mg. X 1 a day and METRONIDAZOL 500 mg. X 2 a day and RIFADIN 300 mg. X 2 a day for the last three months. Now I switched to DOXYLINE 100 mg. X 2 a day and RIFADIN 300 mg. X 2 a day and METRONIDAZOL 500 mg. X 2 a day.



I have had a Hexzimer reaction 5 times until today ,each of them took about a month to end.After the last one swelling start in different parts of my legs which i think because of too many bacteria was dying in my legs .I still have swelling in my feet only which gets smaller every day.I havent had any improvements in my disability yet but progression of ms stopped.I keep taking doxy - rifadin and i will inform you if anything else happens.

I also wonder if anyone else experienced swelling in their leg,please reply me..................
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Postby SarahLonglands » Fri May 13, 2005 4:35 am

This is excellent news! It depends on your disability when you started as to what improvements you might expect, for instance how much damage you have in th spinal chord, where there is less room to make new pathways than in the brain. I was very lucky because for me, it was all in the mind.:wink: All too often people who have had progressive disease for that long, don't improve at all and carry on progressing, so to hear your news is excellent. Perhaps you might consider starting a thread of your own, where it will be easier to keep all your progress notes together.

Quite a few people do get swelling in the legs: with me it was mainly my ankles and feet, but all gone now, eighteen months down the line. I know a young girl, soon to be thirteen, who gets terribly swollen knees and reactive arthritis, whenever she takes metronidizole. She has been on the treatment, for ME in this case, for about a year, and the swelling now gets a bit less every time.

Sarah :)
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Postby yguner » Fri May 13, 2005 9:01 am

Dear Sarah,

Thank you for your reply,i am happy to hear swelling is a good sign.
I also wonder how long it usually takes to eradicate the human body from EB form and RB form of this bacteria.Because the recovery starts after eradication of the bacteria.My lessions are only in my spinal cord,i am not sure if i have an axonal damage,i am 35 year old male and have been using wheelchair for five years.

Sincerly ,

Guner
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Postby SarahLonglands » Sat May 14, 2005 5:36 am

Dear Guner,

I was going to reply to this by private mail, but I thought that since you asked in a public forum I should reply likewise, because it might well help other people. :?

Firstly have you read this in my husband's website, explaining more about the eradication of EB and RB infection?


Chlamydiae have a biphasic life-cycle. A small, infectious, non-replicating extracellular particle (the elementary body, or EB) spreads the infection both between persons and between host cells. On gaining entry to a host cell, the EB is able to transmute into a larger, diffuse form (the reticulate body, or RB) which utilises the host cell’s energy-generating organelles for its own use. It is an energy-parasite. By this means it is able to replicate rapidly, releasing multitudes of EBs into the extracellular milieu. Agents which block protein synthesis, such as doxycycline and roxithromycin, stall this replicating phase, but do not eliminate the intracellular organism.

Chlamydiae are complex organisms. Long ago their ancestors must once have been free-living. They must have possessed their own energy-generating pathways. The transformation from EB to RB is an active change, and an active change implies the retention of at least some of these pathways. The ones with the most utility for this purpose would be anaerobic, and thus susceptible to metronidazole. Metronidazole should kill the organism while it transformed itself from the EB to the RB.



http://www.davidwheldon.co.uk/ms-treatment.html


As to your question about recovery, I would say that it has started as soon as the progression stops. As to the wheelchair, physiotherapy might help. Are you able to walk at all? If so, practising with a walker might also help, because it will build up strength in you leg muscles. Determination also helps greatly and I think you have this, like me, however, at the end of the day, if the damage in your spine is too bad, you might never be able to overcome it and will have to be content with stopping the progression. You will only know by trying, though, so please don't give up. :)

Take care,

Sarah
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Postby yguner » Sat May 14, 2005 8:53 am

Dear Sarah,

I have read your husband's web site many times until now and i wonder if metronidazol kills extracellular EB's as it kills intracellular EB's.The reason i am asking this question is the invention patent 6,579,854 points out extracellular EB's need different medication like succimer (DMSA) or disulfide reducing agent.

During the unique chlamydial life cycle, it is known that metabolically-inactive spore-like EBs are released into the extracellular milieu. Although these released EBs are infectious, they may not immediately infect nearby susceptible host cells until appropriate conditions for EB infectivity are present. The result of this delay in infection is the extracellular accumulation of metabolically-inactive, yet infectious, EBs. This produces a second type of chlamydial persistance referred to herein as EB "tissue/blood load"). This term is similar in concept to HIV load and is defined herein as the number of infectious EBs that reside in the extracellular milieu. Direct microscopic visualization techniques, tissue cell cultures, and polymerase chain reaction test methods have demonstrated that infectious EBs are frequently found in the blood of apparently healthy humans and animals. This phenomenon is clearly of great clinical importance in chlamydial infections as these metabolically-inactive EBs escape the action of current antichlamydial therapy which is directed only against the replicating intracellular forms of Chlamydia. The presence of infectious extracellular EBs after the completion of short term. anti-replicating phase therapy for chlamydial infections has been shown to result in intracellular infection relapse




http://www.pharmcast.com/Patents/Yr2003 ... 061703.htm



I am confused about if we are going to need to take a drug called succimer (DMSA) for extracellular EB's in the near future.
About the question you asked,i cant even stand from my chair at this time because of too much spasm in my legs.
What do you think about killing extracellular EB's, are we going to need to take succimer (DMSA) or not.

Thank you for your time,

Guner
Last edited by yguner on Wed Sep 21, 2005 1:52 am, edited 2 times in total.
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Postby Arron » Sat May 14, 2005 9:47 am

yguner, I split your posts into its own thread so it can be easier to find.

best of luck to you,
-arron
Disclaimer: Any information you find on this site should not be considered medical advice. All decisions should be made with the consent of your doctor, otherwise you are at your own risk.
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Postby SarahLonglands » Sat May 14, 2005 10:57 am

Guner,

Now I'm getting confused! :? DMSA is used in treating chronic lead and mercury poisonings, not CPn infections. David is in regular contact with both Charles Stratton and Ram Sriram and none of this has ever been mentioned. As far as I am aware, the extra-cellular bodies, though infectious are non-replicating. They get into the cells and become reticulate bodies, which are energy parasites and reproduce rapidly, releasing many new EBs into the extracellular environment. This can be stalled by taking doxycycline or somesuch baceristatic antibiotic. So:

Doxycycline and roxithromycin block the replicating phase and may be expected to force the organism to maintain itself by using its own primitive anaerobic respiratory mechanisms. In this suspended state it would be susceptible to anti-anaerobic agents such as metronidazole.


So, basically, the EB load is gradually depleted by using three antibiotics, two bacteristatic ones used together to avoid the developing of resistance, then metronidizole to actually kill the germs as they become RBs and try to exist in an anaerobic environment where they are susceptible to metronidizole.

If, you notice, the patent in your link dates from 2003 and does not mention Metronidizole. This is because although Stratton, the microbiologist, is a firm believer in it, Sriram, the neurologist, is less sure, or at least was then. This is largely because it can make people feel so grotty that they might well give up the treatment prematurely, which as it says in your quote, can cause a relapse. Now, I am no longer taking continuous antibiotics, having stopped after a year, but booster doses of two weeks every two months or so. I have not had a relapse and am quietly improving all the time, so I don't think you need worry at all that something else, especially something like DMSA is going to be added to the Vanderbilt regime, because eventually all the extracellular EBs will be done away with. OK, so you might well get a reinfection at some point, but the hope is that as with vaccination, you would build up a natural immunity to this. :)

Sarah
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Postby yguner » Sat May 14, 2005 1:16 pm

Dear Sarah,


Here is document about succimer (DMSA) and its use in the treatment of Cpn.


As described in previous sections. it is also believed that persistance of chlamydial infections, in part, may be due to the presence of cryptic forms of Chlamydia within the cells. This cryptic intracellular chlamydial form apparently can be activated by certain host factors such as cortisone (Yang et al., Infection and Immunity, 39:655-658 (1983); and Malinverni et al., The Journal of Infectious Diseases, 172:593-594 (1995)). Antichlamydial therapy for chronic Chlamydia infections must be continued until any intracellular EBs or other intracellular cryptic forms have been activated and extracellular EBs have infected host cells. This reactivation/reinfection by chlamydial EBs clearly is undesirable as it prolongs the therapy of chlamydial infections, as well as increases the opportunity for antimicrobial resistance to occur.


Physiochemical agents have been identified that can inactivate chlamydial EBs in their respective hosts by reducing disulfide bonds which maintain the integrity of the outer membrane proteins of the EBs. For Chlamydia, disruption of the outer membrane proteins of EBs thereby initiates the transition of the EB form to the RB form. When this occurs in the acellular milieu where there is no available energy source, the nascent RB perishes or falls victim to the immune system. Thus, disulfide reducing agents that can interfere with this process are suitable as compounds for eliminating EBs.

One such class of disulfide reducing agents are thiol-disulfide exchange agents. Examples of these include, but are not limited to, 2,3-dimercaptosuccinic acid (DMSA; also referred to herein as "succimer"); D,L,-.beta.,.beta.-dimethylcysteine (also known as penicillamine); .beta.-lactam agents (e.g., penicillins, penicillin G, ampicillin and amoxicillin, which produce penicillamine as a degradation product), cycloserine, dithiotreitol, mercaptoethylamine (e.g., mesna, cysteiamine, dimercaptol), N-acetylcysteine, tiopronin, and glutathione. A particularly effective extracellular antichlamydial agent within this class is DMSA which is a chelating agent having four ionizable hydrogens and two highly charged carboxyl groups which prevent its relative passage through human cell membranes. DMSA thus remains in the extracellular fluid where it can readily encounter extracellular EBs. The two thiol (sulfhydryl) groups on the succimer molecule (DMSA) are able to reduce disulfide bonds in the MOMP of EBs located in the extracellular milieu

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Postby Daunted » Sat May 14, 2005 4:21 pm

I am currently taking Amoxicillin, Rifampin, Zithromax + Flagyl. (The Vanderbilt protocol from Charles Stratton as of last fall).

You'll note that amoxicillin is listed in the blurb you posted.
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Postby SarahLonglands » Sun May 15, 2005 4:44 am

Guner,

As Daunted says, he is on the Vanderbilt protocol as of last autumn, not two or three years previously. The important thing about this is that it now includes metronidizole (flagyl) so you need not worry at all that DMSA is going to be added! Also, I'm not imagining that I am getting better, I really am.

Sarah
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Postby yguner » Sun May 15, 2005 6:31 am

Hi Sarah,


Thanks alot for the information you gave me about DMSA ,i am not worrying about it anymore.I will be taking metronidazol with rifadin and doxycycline combination.

Best wishes ...

Guner
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Postby Daunted » Sun May 15, 2005 11:27 am

If you are concerned, do take Amoxicillin as well. I read through the handout I have from my doctor, and it turns out a previous protocol used some of the drugs you mentioned, then they moved to amoxicillin.
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Postby yguner » Mon May 16, 2005 1:05 am

Hi Daunted,


Can you tell me which combination are you taking with amoxicilin and what are the doses in mg.Because i have ppms my bacteria load is huge and i still have too much RB form of bacteria in my body, after clearing RB forms from my body i might switch to amoxicilin combination to manage extracellular EB forms which i must have alot in my body.


Take care,

Guner
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Postby Daunted » Mon May 16, 2005 5:31 am

yguner wrote:Hi Daunted,


Can you tell me which combination are you taking with amoxicilin and what are the doses in mg.Because i have ppms my bacteria load is huge and i still have too much RB form of bacteria in my body, after clearing RB forms from my body i might switch to amoxicilin combination to manage extracellular EB forms which i must have alot in my body.


Take care,

Guner


I'd suggest taking the Amoxicillin, then.

The protocol I am on is:

Amoxicillin 500mg 2x a day
Azithromycin 250mg Mon, Wed, Fri (Can substitute Doxycycline 100mg 2x a day)
Rifampin 300mg 2x a day

and pulses of Metronidazole (500mg 2x a day).

The amoxicillin was actually the first medication I was instructed to start taking, and I'm not sure that there's any reason to wait.

Good luck!

D.
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Postby Daunted » Mon May 16, 2005 5:33 am

yguner wrote:Hi Daunted,


Can you tell me which combination are you taking with amoxicilin and what are the doses in mg.Because i have ppms my bacteria load is huge and i still have too much RB form of bacteria in my body, after clearing RB forms from my body i might switch to amoxicilin combination to manage extracellular EB forms which i must have alot in my body.


Take care,

Guner


I'd suggest taking the Amoxicillin, then.

The protocol I am on is:

Amoxicillin 500mg 2x a day
Rifampin 300mg 2x a day
Azithromycin 250mg Mon, Wed, Fri (Can substitute Doxycycline 100mg 2x a day)

and pulses of Metronidazole (500mg 2x a day).

Good luck!

D.
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