posted
So, everyone remember that whole cure chronic lyme with Diflucan??
I always felt it was a bunch of hoey that Borrelia had a p450 enzyme, but check this out, I wonder why nobody saw this before, because it makes such perfect logic.
1: Parasitology. 2003 Oct;127(Pt 4):311-5. Links Clotrimazole, ketoconazole, and clodinafop-propargyl inhibit the in vitro growth of Babesia bigemina and Babesia bovis (Phylum Apicomplexa).Bork S, Yokoyama N, Matsuo T, Claveria FG, Fujisaki K, Igarashi I. National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada-cho, Obihiro, Hokkaido 080-8555, Japan.
We evaluated the growth inhibitory efficacy of the imidazole derivatives, clotrimazole (CLT) and ketoconazole (KC), and the herbicide clodinafop-propargyl (CP), in in vitro cultures of Babesia bovis and B. bigemina. Clotrimazole was effective in a dose range of 15 to 60 microM (IC50: 11 and 23.5 microM), followed by KC (50 to 100 microM; IC50: 50 and 32 microM) and CP (500 microM; IC50: 265 and 390 microM). In transmission electron microscopy, extensive damage was observed in the cytoplasm of drug-treated parasites. Combinations of CLT/KC, CLT/CP and CLT/KC/CP acted synergistically in both parasites. In contrast, the combination of KC/CP was exclusively effective in B. bovis, but not in B. bigemina.
PMID: 14636017 [PubMed - indexed for MEDLINE]
1: J Parasitol. 2003 Jun;89(3):604-6. Links Clotrimazole, ketoconazole, and clodinafop-propargyl as potent growth inhibitors of equine Babesia parasites during in vitro culture.Bork S, Yokoyama N, Matsuo T, Claveria FG, Fujisaki K, Igarashi I. National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada-cho, Obihiro, Hokkaido 080-8555, Japan.
The antifungal agents clotrimazole (CLT) and ketoconazole (KC) and the herbicide clodinafop-propargyl (CP) inhibit growth of Plasmodium sp., Toxoplasma sp., and Trypanosoma sp. In the present study, we evaluated these drugs against the in vitro growth of the equine protozoan parasites Babesia equi and B. caballi. Clotrimazole (IC50: 2 and 17 microM), KC (IC50: 6 and 22 microM), and CP (IC50: 450 and 354 microM) were effective growth inhibitors. Interestingly, intraerythrocytic KC-treated Babesia sp. were observed to be in immediate contact with the plasma fraction of the blood in electron microscopy. These results demonstrate the babesiacidial activities of these compounds and suggest their chemotherapeutic potential for the treatment of equine babesioses.
PMID: 12880264 [PubMed - indexed for MEDLINE]
These antifungals work through the p450 enzyme, just like Diflucan.
The problem is that no one knows what dose would be effective. Many here have been on the various antifungals (including those mentioned) and have not had any improvement with Lyme or Babesia symptoms as far as I know.
Bea Seibert
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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What I believe is that the antifungals are "helping" by doing something to certain babesia parasites. Also, I have strong objections to the thought that these medications could cure Babesia anyways.
Besides, even if they could, you still have borreliosis, and antifungals don't do anything against that.
Bea, I'm gonna post something else to support my hypothesis regarding the German doctor who was using antifungals for Babesia.
Those who have taken these drugs don't report the same kind of vast improvement, it would seem as those who take very well tested babicidal drugs.
My thinking is that these antifungals exert some effect on certain Babesia species, but not on others as chemotherapy testing has seemingly shown a rather heterogenious pattern of suseptabilty to various Babesia medications.
That was my point, not that we should all be taking Diflucan. My op ed on that info would say that unless you fit the Bab strain perfectly, its likely about as effective against babs as plaquenil. (meaning enough to kinda irritate the protozoa, but certainly not killing)
Posts: 559 | From Cary, NC | Registered: May 2006
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luvs2ride
Frequent Contributor (1K+ posts)
Member # 8090
posted
I always felt the Diflucan worked because your problem was really yeast, not lyme. Symptoms are the same.
-------------------- When the Power of Love overcomes the Love of Power, there will be Peace. Posts: 3038 | From america | Registered: Oct 2005
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5dana8
Frequent Contributor (1K+ posts)
Member # 7935
posted
I agree with luvs2ride
Many of the lyme symptoms are the same as yeast. My instinct says it may boil down to that.
Knocking the yeast symptoms may help alot but you would still be left with the lyme.
I hope I am wrong. It would be nice to think it is this easy.
-------------------- 5dana8 Posts: 4432 | From some where over the rainbow | Registered: Sep 2005
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GiGi
Frequent Contributor (5K+ posts)
Member # 259
posted
Do you think Schardt is wrong/lying/just not saying it's babs cause he doesn't now any better?
Posts: 298 | From los angeles | Registered: Mar 2006
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bettyg
Unregistered
posted
lymescience, how about editing your topic line showing DIFLUCAN in it so those of us who have/were on diflucan can read this? Thank you!
I was on diflucan 13 months; NO improvment at all. Bettyg
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posted
It was my understanding that this is a treatment for Lyme, not Babesiosis.
Also, it is a two step protocol.....not Diflucan alone. Dr S recommends 50 days of Diflucan, which weakens the Lyme bacteria, followed by 20 or 30 days of penicillin to kill the bacteria.
For long term cases of Lyme, treatment may have to be repeated a couple times.
Posts: 4638 | From South Carolina | Registered: Mar 2001
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posted
Someone correct me if I am wrong, but don't Flagyl and Tini both also inhibit the P450 enzyme?
There is also research out there that showed that the "azoles",of which diflucan etc. are members, turned resistant helicobacter pylori into non-resistant killable bugs.
Anyway, I vote for flagyl and tini--inhibits the P450 and busts those cysts.
Posts: 554 | From Naples, Italy | Registered: Jun 2006
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Jellybelly
Frequent Contributor (1K+ posts)
Member # 7142
posted
In my case, there may be something to this. If the antifungals are just working on yeast then what would explain, the different reactions I have to various antifungals?
I only know them by Nizoral and Diflucan, but I have taken them both. Are they supposed to both work on Babesia or primarily the Diflucan?
I have had progress in the past with Nizoral, but no real serious herxing. Because of that my LLMD said lets try Diflucan, cause maybe yeast is a real big problem for you. I was put on Diflucan and I thought I was going to die. Herx was horrible. We backed me down to about 50 mgs every other day, still couldn't do it. I was on it a total of about 10 days. The herx was bad, but progress was not really noticable. Was it because I couldn't stay on long enough? I have been sick a very long time.
There is a difference in how each of these antifungals work on me, that much I know for sure. Is one different because it has an effect on Babesia?
Posts: 1251 | From california | Registered: Apr 2005
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posted
My reasoning?? There is direct science for these antifungals and Babesia, though while not killing them, seems to **** them off.
There's more research than I was even aware until I started reading more about Babs.
The Japanese research the subject quite a bit, seems money is involved in the horse industry there.
Here's a tidbit of knock on the ole crazy unification theory for ya, statins, which lower LDL cholesterol also inhibit Babesia because they remove a source of food for the parasite.
Anyone remember the treatment of "Lyme" with cholestramine? Supposedly this was lowering the nuerotoxins, but made everyone real sick if they had Lyme and took this med.
Same kinda thing seems to happen with Diflucan.... huh, interesting, perhaps, being as though there is direct evidence for both mechanisms using hard science, ie: the P450 enzyme (by the way if it worked on Lyme, then the Flagly, of which I was unware had effects on the p450 enzyme, right not I think not, but I'll look that up, it had no effect on the spirochetal Lyme), and the lowering of LDL cholesterol (which if you look up Cholestramine, you'll find that lowing the LDL is exactly what the drug does.........kinda coincidental don't ya think, that two people treating "Lyme" in an unconvential way, also happen to be using agents that also have activity proven against Babesia, yet there remains no real science regaring these drugs against Lyme???
Posts: 559 | From Cary, NC | Registered: May 2006
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posted
My conclusions: these drugs have a mild effect on the clinical treatment of Babs, which if followed pricisly, may help the immune system to finally knock out the Babs.
My real theory: Babs is the reason we are all still sick. It changes the immune system when it sticks to your blood vessels.
We all still have the Lyme, and probally the Bart, but the reason we can't get rid of the freaking Lyme is because those gosh darned Babs don't want to freaking die, and if they didn't wan to stick to a very particular vein, we wouldn't be having this whole chronic lyme thing in the first place.
I just starting reading stuff regarding this vein, so, I'm not 100 percent convinced, but it looks extremely promising, and probable considering the evidence.
I'll post some info about this vein soon. Right now, its pretty difficult reading, and I'm not certain I understand all of it.
Posts: 559 | From Cary, NC | Registered: May 2006
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oxygenbabe
Frequent Contributor (1K+ posts)
Member # 5831
posted
They are also studying an antihistamine, astemizole, as it inhibits malaria. It was taken off the market. They'll need to develop less toxic versions.
If they could do a drug screen of all existing drugs for babesia they might get some good info. This is something I meant to follow up on last year but got distracted. There is a scientist doing this for malaria and other major killers. It would be nice to interest him in babesia but it is not nearly as widespread or obvious as malaria.
One area of interest would be weedkillers and similar drugs as babesia has an apicoplast--an organelle. Do some research and you'll see. Since that is a very ancient aspect of babesia and there are lots of weedkillers out there, it would be a good avenue of research to develop ones we could tolerate orally. They might kill babs.
Posts: 2276 | From united states | Registered: Jun 2004
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Jellybelly
Frequent Contributor (1K+ posts)
Member # 7142
posted
Interesting what you say about Babs sticking to the walls of viens. I have never read about how Babs functions or survives, but just that little bit of info makes me wonder if their liking viens is the reason Heparin seems to kill it according to that study out of Japan.
At my sickest I had very large numbers of symptoms associated with Babesia. By the time I started looking into Lyme again I had already been on heparin for 3 1/2-4 years. I had also used ABX some. I was in 85-90% remission before I was tested for any of this stuff. My Babs came back negative.
Maybe the heparin had managed to pry it off the walls of the viens and expose it to the ABX and my own immune system.
YET ANOTHER REASON TO CONSIDER HEPARIN.
National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada-cho, Obihiro, Hokkaido 080-8555, Japan.
We examined the inhibitory effects of three heparins on the growth of Babesia parasites. The multiplication of Babesia bovis, B. bigemina, B. equi, and B. caballi in in vitro cultures and that of B. microti in vivo were significantly inhibited in the presence of heparins, as determined by light microscopy. Treatment with various concentrations of heparin showed complete clearance of the intracellular parasites. Interestingly, a higher percentage of abnormally multidividing B. bovis parasites was observed in the presence of low concentrations of heparin. Furthermore, fluorescein isothiocyanate-labeled heparin was preferably found on the surfaces of extracellular merozoites, as detected by confocal laser scanning microscopy. These findings indicate that the heparin covers the surfaces of babesial merozoites and inhibits their subsequent invasion of erythrocytes.
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