randibear
Honored Contributor (10K+ posts)
Member # 11290
posted
can someone please explain why some drugs, say doxy, work for early lyme and not late lyme?
why prescribe biaxin for late stage and not early?
is it because the drugs do different things?
-------------------- do not look back when the only course is forward Posts: 12262 | From texas | Registered: Mar 2007
| IP: Logged |
Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
RandiB...
Doxy is often prescribed for early Lyme not just for its affect on the Lyme bacteria... but to address Ehrlichiosis, RMSF, Bartonella and other tick borne diseases.
Babesia is one that would require a different class of drugs.
There are other more complex reasons that could be thrown in the explanation... but this is all I have energy and brain power for right now.
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
In some ways, anthrax is a lot like borrelia burgdorferi.
(LF = lethal factor)
"Bacillus anthracis ("anthrax") is a proven agent of biological terrorism. Pulmonary anthrax, in which spores of the anthrax bacteria are inhaled, is typically fatal
***unless diagnosis is made at an early stage of infection, when antibiotics such as Ciprofloxacin can provide a complete cure.***
***At late stages in the disease, antibiotics can kill the anthrax bacteria, but do not affect LF secreted by the bacteria***, which is sufficiently concentrated in the bloodstream.
LF enters cells and inactivates a human protein called "mitogen-activated protein kinase", or "MAPKK", disrupting the normal signaling pathways of the cell and inducing cell-death."
Bb looks to cleave (break apart) MAPKK-1.
The newest drug to prevent anthrax/ combat the toxin...not yet on the market...prevents this cleaving.
"In the cytoplasm, LF acts as a protease that cleaves MAP kinase kinase (MAPKK 1 and MAPKK 2), inhibiting pathways that
***rely on this kinase family and causing cell death.***"
If MAPKK-1 is inhibited (missing 'cause the toxin breaks it down) and the cell *can't/doesn't die*...
Up go TNF alpha and IL1B to try to destroy the infected cell.
If we destroy the cell in which Bb is camped out, is Bb then destroyed also, or is it once again "set free"?
Keep in mind too, that while antibiotics (and our own antibodies) can destroy the cell walls, this does not destroy Bb because Bb has the ability to rebuild its cell walls.
Doxy HELPS, but does not cure. By binding Ca, it too maybe inhibiting PKC (a calcium activated protein kinase).
The Salp 15 protein (from the tick's saliva) helps Bb to invade because it interfers with CALCIUM fluxes.
Since our cells need calcium (and of course the other electrolytes which go in and out of our cells all the time really fast), our body will likely over-ride the ability of doxy and will pull additional Ca out of storage to help.
We look to be trying to counter Bb's PKC INHIBITOR...a *calcium activated* protein kinase.
It appears our body wants PKC to "be there", not inhibited.
A protein kinase is a kinase enzyme that modifies other proteins by chemically ***adding phosphate groups to them ***(phosphorylation).
Bb's toxin looks to be removing phosphates from 2 serines preventing a transfer onto an amino acid that is supposed to be happening.
We need calcium to remain in the infected cells for a tad longer and not be "exported"...so that PKC, the calcium activated protein kinase can work.
Close the TRPM8 channel. Watch it happen on the animated link I've provided re: photon transfer -> transducin -> gates "close" and Na and Ca are "stuck" in the cell.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
| IP: Logged |
randibear
Honored Contributor (10K+ posts)
Member # 11290
posted
is there a drug on the market or being developed that WILL destroy the cell wall and the nucleus and cause it to die?
-------------------- do not look back when the only course is forward Posts: 12262 | From texas | Registered: Mar 2007
| IP: Logged |
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
A brand new drug to prevent the anthrax toxin from cleaving MAPKK-1 might work.
It is not yet on the market.
Gallium maltolate (also not available yet) may also work from other angles.
Meanwhile, in Romania a few years ago, doctors cured lyme using abx AND restored Mg levels.
Electromagnetic therapy (Rife/far infrared) AND MgCl appear to help.
"Magnesium blocks the loss of protein kinase C, leads to a transient translocation of PKC(alpha) and PKC(epsilon), and improves recovery after anoxia in rat hippocampal slices."
AND Mg is needed by our antibodies to deal with Bb's OspB.
AND Mg INactivates HMG CoA reductase and halts cholesterol production (which is one of the pathways Bb is taking to build its cell walls).
AND Mg is an anti-inflammatory and anti-histamine.
AND (gets complex but impacts the insulin receptor):
"magnesium is an essential activator of ERK2"
MAP kinases, also known as extracellular signal-regulated kinases (ERKs)
MAPK2 = Extracellular signal-regulated kinase 2
MAPK2 (p42/ERK2) is the best characterized signalling module and is usually activated in response to mitogens.
A mitogen is a chemical substance, usually some form of a protein, that encourages a cell to commence cell division, triggering mitosis.
The ***tyrosine-phosphorylated*** band corresponds to p42MAPK2 (erk2).
Phosphorylation of src tyrosine kinase (pronounced "sarc") by C-terminal Src kinase (Csk) induces a conformational change in the enzyme, resulting in a fold in the structure, which masks its kinase domain, and
is thus shut "off"
"Tyrosine phosphorylation of type I insulin-like growth factor receptor (IGF-IR) is one of the early responses to potent mitogenic stimuli insulin-like-growth factor 1 (IGF-I).
This receptor binds IGF-I with high affinity to activate cellular proliferation in both normal growth and development and malignant transformation and has tyrosine kinase activity.
The IGF-I receptor plays a critical role in transformation events.
It is highly over expressed in most malignant tissues where it functions as an
anti-apoptotic agent by enhancing cell survival.
IGF-I signals are mediated via phosphorylation of a family of insulin receptor substrate proteins (IRS), which may serve both complementary and overlapping functions to insulin receptor (IR) in the cell."
Bb is PFK dependent. Insulin activates both forms of PFK (1 and 2).
[ 05-02-2009, 08:01 PM: Message edited by: Marnie ]
Posts: 9424 | From Sunshine State | Registered: Mar 2001
| IP: Logged |
posted
Doxy works fine for me - Doxy at a high dose did more for me than any other ABX, and I definitely had late-stage lyme with many neurological problems. I would be lost without my Doxy!
ESG
Posts: 424 | From Connecticut, USA | Registered: Nov 2003
| IP: Logged |
posted
My LLND says doxy is effective in all stages and may even be somewhat effective for babesia. I wonder if differences have more to do with the person, or the strain of pathogen than the antibiotic.
Posts: 199 | From utah | Registered: Jan 2009
| IP: Logged |
'Kete-tracker
Frequent Contributor (1K+ posts)
Member # 17189
posted
Someone may've simplified it too much somewhere or made assumptions. Doxycyline is quite often used for late-stage Lyme. Just at higher levels (maybe 400mg/day) & for extended (2-4) month periods, after which the improvements tend to drop off, neccessitating a switch in class (family) of abx.
Doxy's often used First as it's effective against some co-infections. Other drugs, like Biaxin (a "macrolide"), are also effective at all stages against Lyme borrelia. It's just that one uses the simpler abx (doxy/amoxy) as a general rule when one can. Very effective at erradicating the new body pathogen & less chance of complications, like GI tract issues.
The protocol is much shorter for early Lyme: 4-6 weeks vs. 4 - 6 months (minimum) for disseminated Lyme (& often up to 2 years). Some even need ongoing antibiotic therapy, esp. when they've been untreated for many years & have CNS issues, in order to be functional. (See Dr B's comments in U.O.S.)
Bootm line- There really is no seperate list of abx for early vs. late-stage Lyme, randi.
Posts: 1233 | From Dover, NH | Registered: Sep 2008
| IP: Logged |
kreynolds
Frequent Contributor (1K+ posts)
Member # 15117
posted
I have been on about 6 different IV ABX's. The one I always rely on is IV Doxy.
I have tried Tygacil,Invanz,Rocephin,Penicillin,Vancomycin,and Clindamycin.
If I had to choose the top 2 for myself it would be IV Doxy or IV Tygacil.
I am on 300 mg/day of IV Doxy... strong stuff.
-------------------- Diagnosed CDC + 6/2007
Quest: + IGG Bands 18,23,39,41,58,66 and 93.
Quest: + IGM Bands 23,39
Quest: + Bartonella (B.Henselea & B. Quintana),+ Babesia, and + Mycoplasma and Lyme-Induced Addisons Disease
+ Biofilm blood test 12/2010 Posts: 1185 | From New York | Registered: Apr 2008
| IP: Logged |
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
My sis zoomed to stage 3 lyme after being misdiagnosed originally and given steroids for "RA".
NONSTOP abx for 3 years (including IV) along with Mepron and Azith (though never formally dx'd to need it) did not stop the ongoing destruction of her joints.
Bb has a gene to EXPORT Ca from the cell. It does not want Ca to go in the cell.
And Doxy binds Ca.
Do you think the body will try to over-ride this and continue to pull the nutrients it needs out of storage?
The TRPM8 channel is active. This channel involves Na and Ca. Ca is exported.
This is the channel we must temporarily block.
The video of this happening (photon transfer -> transducin = a G helper protein -> "doors" closing (keeping Na and Ca IN the cell) is here:
Scroll down a little and watch for the blue box on the left side.
You may have to use your computer tools to make that bright blue box bigger.
On the left side...the word, "Photon" will appear in white as the animation goes on.
Look for the word, transducin to appear in the middle of the event.
Notice what happens to the Na-Ca channel on the right.
It closes.
Bb has a PKC inhibitor.
C = calcium activated P = protein K = kinase = phosphate transfer
Bb is INHBITING this calcium activated...
In the cells it is infecting i.e., our defense cells.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
| IP: Logged |
randibear
Honored Contributor (10K+ posts)
Member # 11290
posted
hmm, my sister has rheumatoid arthritis. i'm pretty sure it's lyme and she just finished about a month of steroids and now is going to some speialist.
-------------------- do not look back when the only course is forward Posts: 12262 | From texas | Registered: Mar 2007
| IP: Logged |
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
![[Big Grin]](biggrin.gif)
![[Wink]](wink.gif)
It's just that one uses the simpler abx (doxy/amoxy) as a general rule when one can. Very effective at erradicating the new body pathogen & less chance of complications, like GI tract issues.
Printer-friendly view of this topic