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08/05/2011 07:53 PM

Tindamax

i70pb
i70pb  
Posts: 209
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Has anyone been on the new drug Tindamax ? Your thought & info welcome please.
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08/05/2011 08:00 PM
lymeinmich
 
Posts: 1094
Member

shorelinelyme just mentioned tindamax in the post under "DOXY"

I was going to google it.


08/05/2011 10:22 PM
Bettyg
 
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I'm an Advocate

An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to tinidazole.

Int Microbiol. 2004 Jun;7(2):139-42.

An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to tinidazole.

Brorson O, Brorson SH.

Source

Department of Microbiology, Vestfold Sentralsykehus, T√łnsberg, Norway.

Abstract

The susceptibility of mobile and cystic forms of Borrelia burgdorferi to tinidazole (TZ) was examined.

The minimal bactericidal concentration (MBC) of TZ against the mobile spirochetes was >128 microg/ml at 37 degrees C in micro-oxic atmosphere when incubated for 14 days.

TZ significantly reduced the conversion of mobile spirochetes to cystic forms during incubation.

The MBC for older (10-months-old) cysts at 37 degrees C in a micro-oxic atmosphere was >0.5 microg/ml, but >0.125 microg/ml for young (1-day-old) cysts.

Acridine orange staining, dark-field microscopy and transmission electron microscopy revealed that, when the concentration of TZ was > or = MBC, the contents of the cysts were partly degraded, core structures did not develop inside the young cysts, and the amount of RNA in these cysts decreased significantly.

When cysts were exposed to TZ, both the spirochetal structures and core structures inside the cysts dissolved, and the production of blebs was significantly reduced.

These observations may be valuable in the treatment of resistant infections caused by B. burgdorferi, and suggest that a combination of TZ and a macrolide antibiotic could eradicate both cystic and mobile forms of B. burgdorferi.

PMID: 15248163 [PubMed - indexed for MEDLINE]

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http://www.ncbi.nlm.nih.gov/pubmed?term=Brorson%20AND% 20Tinidazole

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National Center for Biotechnology Information, U.S. National Library of Medicine8600 Rockville Pike, BethesdaMD, 20894USA


08/05/2011 10:22 PM
ontong
ontongPosts: 269
Member

hi, I am on Tindamax as well as IV rocephin. I was doing ok with rocephin, but three days after starting Tindamax I had unbelievable herxing, at a level that I felt I simply needed to be hospitalized. I am on every kind of detox, herbal remedy, vitamin regimen, etc, but I could only manage the pain with several hydrocodone. My doc is telling me this is good news, that the Tindamax has found a new "veign" of bacteria, but OMG the pain and debilitation has been staggering. I eventually had to stop the Tindamax for a week and have restarted on a very low dose.

So, apparently it can be very effective at busting cysts, but really nailed me good.

John


08/05/2011 10:39 PM
Bettyg
 
Posts: 33641
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Eva Sapi's recent research calls into question everything we thought we knew about Lyme "cysts." In fact it destroys the old thinking.

http://lymemd.blogspot.com/2011/07/everything-you-thought- you-knew-about.html

quote:

We have heard about cell wall antibiotics, intracellular antibiotics and cyst-busters. Think again.

She investigated the effect of various antibiotics on Lyme spirochetes and round body forms - also know as cystic forms.

Doxycycline worked according to plan. Doxy inhibits protein synthesis - it kills bacteria, including Lyme, by action within the cytoplasm, inhibiting the manufacture of proteins required for the bacteria's survival.

Doxy and others are commonly referred to as intracellular antibiotics.

Spirochete loads decreased by about 90% while cyst levels increased by 200% - just as expected.

Then amoxicillin data was presented.

Amoxicillin inhibits the formation of bacterial cell walls. Amox and similar drugs should then only be effective in killing spirochetes with an intact cell wall. This is where the results start deviating from the plotted course.

Amoxicillin killed 90% of spirochete forms - OK, but -- it also killed 68% of the cystic forms! Amoxicillin and other cell wall drugs are not cyst busters - only specific anti-parasite drugs kill cysts - or so we thought.

Well lets think again for a second: what are cysts?

Are they balled up forms of spirochetes with a different kind of membrane - or blebs (also described) expressed through the spirochete membrane?

Maybe the former retain much of the cell wall from the original spirochete - maybe that is why amoxicillin works here.

This would seem to clear up a nagging question raised by others. Are cysts and L-forms really the same thing?

These results show that cysts cannot represent a version of L-forms or spheroplasts which result when gram negatives shed their cell walls.

If this were the case a cell wall drug would be ineffective.

Cysts and L-forms are distinct and different forms.

(There may be a hole in this reasoning. I will explain later).

OK So we have learned something new: cell wall antibiotics can also kill some cyst forms which are not L-forms.

Let's look at some more data.

Tigecyline is a not a cyst drug either. Wrong. Tigecycline kills 90% of spirochetes, good so far, but it also kills 90% of cysts!

Tigecycline is an intracellular antibiotic similar to doxycycline! Another fly in the ointment.

OK. Cysts with their lower metabolic rate, still need ribosomal proteins to survive, just not at the levels of intact spirochetes.

Tigecyline is a more powerful drug, higher levels are delivered into the cytoplasm of the cysts. This makes sense.

Cyst forms are still essentially a pleomorphic version of Lyme bacteria with somewhat different features.

In this scenario, cysts could be L-forms. But we have already shown that this is not true because amoxicillin can kill them. Right?

Amoxil is a cell wall drug. I thought so.

Kersten, (antimicrobial agents and chemotherapy, May 1995, p. 1127-1133) states that Beta-lactam antibiotics, which include amox, penicillin and Rocephin, have been shown to cause a specific loss of total intracellular RNA in the absence of cell wall hydrolysis.

In other words, amoxil could possibly work in part as an intracellular agent.

If this is right cyst forms of Lyme could still be L-forms.

So perhaps we have not shown that L-forms and cyst forms are different after all.

The question remains unanswered.

Let's get to the Cyst-busters.

It takes antiparasitic drugs, so we thought, to kill the cysts. Cyst-busters, anti-parasite drugs, kill parasites (and Lyme cysts) not bacteria.

The so called cyst-busters were heretofore used in combination or cycled with other antibiotics.

Previous thinking was that typical antibiotics would kill spirochetes and/or L-forms and that cyst busters would disrupt only the cystic forms.

Cyst-busters do not kill intact spirochetes - so we are told. Very wrong this time.

I cannot cover the whole Sapi study.

The most exciting finding is that Tindamax (tinidazole) - our premier Cyst-buster, is the most effective drug overall.

This "cyst-buster" kills 90% of cysts and spirochetes: by far the best drug. We don't know it's effect on L-forms, but we can guess.

Tindamax probably works by an intracellular mechanism.

If this is true it should be equally effective against L-forms.

It gets even better. Tindamax is the only drug which does a great job on biofilm colonies as well!

(not to be discussed now). More on biofilms later.

Tindamax passes the blood brain barrier and penetrates well into most tissues.

It has been effective in my patients with neurocognitive deficits - neuroborreliosis.

Recently I tried it on another sort of patient. This patient has had intractable Lyme arthritis of his knees.

This young athlete had been extensively treated with IV Rocephin followed by a year of typical oral antibiotics.

Knee effusions have persisted - until I prescribed Tindamax.

Now, after two months, the fluid in his knees has evaporated. His knees are dry and painless for the first time in over one year.

This raises the question: should Tindamax be used as mono-therapy?

Well, I cannot endorse blanket use at this time.

Tindamax has a black box warning. It has been associated with cancer in some laboratory animals.

Perhaps there are more compelling reasons to use Tindamax, but this will have to wait for another post.

My nagging question:

Why does penicillin kill Lyme? It shouldn't.

Lyme is a gram negative bacteria.

While certain Beta-lactam antibiotics can kill gram negative bacteria, penicillin cannot.

Penicillin is only active against gram positive bacteria.

Maybe this other mechanism alluded to above, the alternative intracellular RNA mechanism is significant and explains why penicillin kills Lyme spirochetes. Maybe not.

We need to continually reevaluate things which we have assumed to be true, because many of them are not.


08/05/2011 10:52 PM
Sharon2011
Posts: 18
New Member

I have been recently diagnosed with Lyme. My LLMD wants me soley on tindemax for 3 months. one week on, and one week off. My hubby wants a second opinion on this. If we go this route, I will keep you ball posted.

08/05/2011 10:58 PM
beensLYMEd
beensLYMEd  
Posts: 235
Member

Wow

Thanks


12/28/2011 09:28 PM
kimjgoodwin
 
Posts: 68
Member

Tindamax first month some herxing as with any med switch but it made me about 80% better in 2months with 10 months of treatment. It is worth the first month to benefit after. It kills lyme, biofilm, cysts, bart and babesia. It is the drug i think all lymies have to be on. You pulse with it so you get breaks. I do 3 days on 4 days off some do longer periods 2 or 3 weeks on than off the same length of time.

I saw the person above after 3 years of diagnosis and not better. I was surprised you were ony taking 200 mg of doxy i can see first 2 months of treatment but most people are taking 2 to 4 large doses of antibiotics with lots of natural things and probiotics. If this dr has not improved this you need a new llmd asap.

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