Research from Dr. Zhang’s lab at JH shatters numerous company iconic beliefs about Lyme therapies.
We discern that Lyme disease, or rather the causative organism, Borrelia burdorferi, is very hard eradicate. In vitro (in a standard tube) it took a combination of 3 antibiotics to carry the task. Doxycycline was a claim. The other drugs are either unavailable or prohibitively wasteful, (cefoperazone and daptomycin).
Persistent viability of the spirochete relates to its cap~ to form round body forms and other pleomorphic variants and to from aggregates of spirochetes protected ~ dint of. a muccopolysaccharide covering. Rather that the articles of agreement: L forms, cyst forms and biofilm colonies, Dr. Zhang simplifies: in that place are two groups,rapidly dividing forms (spirochetes) and quiescent forms (persisters).
Cocktails of drugs are needed to extirpate the organism. At this point we comprehend little about the synergy of many combinations.
First off, this is not strange, but Lyme does not form L-forms. L forms are bacterial lacking a confined apartment wall, like mycoplasma. Alternatively, some gram negative bacteria, treated with antibiotics pour out their cells walls transforming into L forms. L forms cannot outlive outside the milieu of the intracellular cytoplasm of the landlord cells. Lyme spirochetes are encased in a dual membrane, not a enclosed space wall. Although the bacteria may possess an intracellular location they are in a primary manner extracellular. Cell wall drugs work for the cause that the Lyme spirochetes have something like some internal skeleton comprised of cell wall stuff, peptidoglycans. Lyme does not form faithful cysts. The terms round body shape and pleomorphic variants is more true.
I don’t like the season cyst busters (always reminds me of departed spirit busters). It may be easier to contemplate Lyme as a dichotomy of spirochetes and persisters.
I am sorry that I have bored you in such a manner far. The rest may be of greater affect.
Doxycycline remains the first line when it comes to treating spirochete forms. Doxy has no impact on stationary forms. You even now knew this.
Flagyl is not a “cyst buster.” It does not put to death stationary forms any better than doxycycline. ( you in all probability did not know this) This in addition true for amoxicillin. Ceftin does consider the ability to kill both laborious and stationary forms of Lyme. Rifampin does not carry off Lyme by itself but confers persister killing movables to doxycycline and amoxicillin.
I was safe that Tindamax must kill stationary forms. It works to such a degree well in the clinical setting. So I asked Dr. Zhang and he responded. Unpublished premises show that Tindamax is ineffective opposed to stationary form of Lyme, perhaps little better than Flagyl. How could I be so wrong?
Then there is a drawn out list of drugs that kill Lyme with greater advantage than currently used drugs, at minutest in a test tube. Two drugs stand away: Diflucan and Artemisinin.
Why do Flagyl and Tindamax be so well? These drugs have thoroughly good penetration into tissues and into the brain. Perhaps this property and synergy reduce to law clinical effectiveness. Tindamax (one of my favorites) is known to boil down in bodily fluids and tissues extremely well.
Doctors regard added Flagyl and Tindamax to Omnicef and Ceftin – since decades, because they are “sac busters.” These doctors had unfair the whole time. It was for ever the other way around.
Ceftin productions a highly touted Lyme drug. It is said to be the only second people of the same age cephalosporin that penetrates the blood brain barricade. Omnicef is a third generation cephalosporin, like Rocephin. All third part generation drugs can pass through the BBB. Early studies cited in the erudition proved that Ceftin was effective in treating betimes Lyme patients with EM rash. It was not closely examined for late state Lyme disease, dissimilar doxycycline.
All cephalosporins do a destitute job of getting into the brain. They sole penetrate the brain when there is influential inflammation in the meninges (lining in a circle the brain). Oral drugs like Ceftin and Omnicef possess poor uptake into the brain in patients by chronic Lyme encephalopathy. Tindamax and Flagyl may not despatch persisters better than the others nevertheless they penetrate hard to reach places including the brain.
Amoxicillin, which like Ceftin/Omnicef does not make away with persisters but amoxicillin has slightly wagerer penetration into the brain/central fearful system. I have found it greater amount of effective in most patients.
Then we are left with the question: how do we deprive of life Lyme persisters in the brain?
IV Rocephin, through adequate brain penetration does have anti-persister properties. Perhaps IV Ceftin (cefuroxime) Zinacef, works more good – worth a try.
Obvioiusly we can’t commission IV antibiotics for everybody.
Rifampin trials the BBB well and should boost the anti-persister effectiveness of drugs in the same state as doxycycline. I have found this clinically to exist the case.
Test tube results to not for aye translate into clinical results. Sulfa drugs deprive of life persister and penetrate well into the brain; clinical effectiveness in my practice has been lacking.
What in regard to Diflucan? penetrates well into the brain and kills persisters. Role in Lyme to exist determined.
Artemisinin? This drug has a concise half-life. This is why a derivative combined with a longer acting doer (Coartem) has greater efficacy for miasm/babesiosis. Artemisinin has unclouded brain penetration. It has activity in preparation for Lyme persisters. Clinical use for Lyme nameless.
We had a lot of inanity wrong but new doors have been opened as the search for the best route to treat Lyme goes on.
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