I have m. pneumoniae and I just found out I also have Babesia. For babs I'm taking mepron now.
I've been treated for m. pneumoniae for almost 9 months and I still have it!
Does anyone know if one can test negative for co-infections at some point?
What helps m. pneumoniae go away???
Thanks, I'm losing hope here . . . Posted by Lymetoo (Member # 743) on :
quote:Originally posted by SAK: Does anyone know if one can test negative for co-infections at some point?
[/QB]
Yes, but don't rely on test results to determine if you're in the clear. Rely on how you feel.
as for the mp...I don't know...sorry!
Hope you kick this soon!!
Posted by SForsgren (Member # 7686) on :
It definitely can be a challenge. Mine are going down, but I am not certain that they are gone yet. In fact, I think it is unlikely. Also depends on how you test. For mycoplasma, PCR is used which is clear indication that the bugs are still there. With antibody tests, the bugs can be gone and it may take a few months for the antibody levels to actually go down. Keep fighting!
Posted by lou (Member # 81) on :
I was under the impression that a person's antibody tests were not necessaily a sign of active infection, and these antibodies could stick around for a long time. This is sometimes called a serological scar. If antibodies did not remain after an exposure to a foreign pathogen, vaccination would not work.
So, what kind of tests are you talking about here?
Posted by Mathias (Member # 5298) on :
Only a PCR test can determine if you still have an infection or not and even that is 100% reliable. Symptoms are a better predictor.
Posted by SForsgren (Member # 7686) on :
The information that I have gotten from the various conferences is that with the Lyme co-infections you generally keep after them until the antibody serologies resort to negative levels. That is how my LLMD approaches it and what I have learned from other LLMD presentations. It is also my personal experience that with continued treatment the levels do go down as I am now nearing the negative ranges on things that were previously quite high.
Posted by christelleny (Member # 6719) on :
I've had mycoplasma pneumonia as a secondary infection for...well, I'm not sure how long, just a very long time.
My doctor told me that it will always show in the analysis (It's air borne, so it's not a rare infection) but the count will come down.
That's what's been happening with treatment.
My count goes up and down, but it never went back to the very high count I had before I began treatment.
I haven't had a pneumonia since I began abx.
Posted by Marnie (Member # 773) on :
It is an ongoing battle while Bb is present.
Bb forces sugar to go into the cells. Most other pathogens also like sugar (not so different from us!). In addition, Bb is capable of breaking down H2O2 inside the endothelial cells using 2 our our 3 antioxidant enzymes to do so. Normally, H2O2 is capable of killing most pathogens. This is what normally helps us to stay healthy 'cause we are fighting germs we can't see every second of our lives.
Bb provides the perfect "home" for many other pathogens...lots of sugar, no H2O2.
IMO...Bb is the pathogen we need to go after first. Get the leader of the pack, so to speak.
Bb is very, very unique. It's outer cell wall is Zn+cholesterol. Almost every other pathogen has an LPS (think sugar) cell wall. Bb follows the cholesterol AND glycolysis pathways. We have to INactivate an enzyme, called HMG CoA reductase to shut off excess cholesterol production in the liver in order to knock out this infection.
This is where the "Marshall protocol" or high doses of Mg - sustained - comes in.
Cholesterol lowering drugs AND magnesium INactivate that enzyme. Cholesterol lowering drugs also can deplete CoQ10, so it is important to take this while/if on them.
Unfortunately it takes HIGH doses for this to work...doses that are not "approved" as yet.
Antibiotics are the wrong class of drugs to use to knock out Bb, IMO.
It is a "triage" situation. Gotta focus on the primary problem, which IS the presence of Bb.
THEN the "traditional" drugs can knock out the remaining infections...if they remain behind.
P.S. Bb looks to incorporate cholesterol in its outer cell wall...mycoplasms in their cell MEMBRANE.
"Gil Ben-Menachem, Ph.D. - NICHD A Newly Discovered Cholesteryl Galactoside from Borrelia Burgdorferi Lyme disease, caused by the spirochete Borrelia burgdorferi, is recognized as a cause of common and serious systemic disease worldwide. It affects the skin, joints, nervous system, and heart, and in its chronic form, can result in autoimmune manifestations such as arthritis.
Lyme disease is the number one vector borne disease, and about 20,000 new cases are reported each year in the US. Little information exists about the protective antigen/s or the host factor/s that confer immunity to B. burgdorferi. The licensed vaccine, composed of a derivative of an outer membrane protein, has been withdrawn by the manufacturer.
Our initial aim was to isolate LPS from B. burgdorferi, for a potential vaccine use. Although LPS has been identified in several spirochaetales, such as Leptospira and Treponema, we could not find evidence for its presence in B. burgdorferi, nor were we able to detect markers of LPS such as KDO, Lipid A or 3-hydroxy fatty acids.
However, we isolated and characterized, two major glycolipids from B. burgdorferi, designated as BbGL-I and BbGL-II. These compounds were purified by silica gel chromatography, and analyzed using GLC-MS, MALDI-TOF, FAB-MS, NMR spectrometry, and metabolic labeling. The structure of BbGL-I was determined as cholesteryl 6-O-acyl-beta-D-galactopyranoside, and that of BbGL-II as 1,2-di-O-acyl-3-O-alfa-D-galactopyranosyl-sn-glycerol.
This is the first demonstration of a cholesteryl galactoside in bacteria. Surprisingly, despite their small size, BbGL-I and BbGL-II elicited antibodies in mice and rabbits, mostly of the IgM isotype. Antibodies to these glycolipids have also been found in sera of Lyme disease patients. The lack of LPS, the abundance of BbGL-I and BbGL-II in the bacterial membrane, their surface exposure (as indicated by fluorescence labeling), and their three-domain structure, lead us to suggest that these glycolipids may assume LPS function."
[ 24. May 2006, 11:15 AM: Message edited by: Marnie ]
Posted by Mathias (Member # 5298) on :
Mycoplasma has no cell wall.
Posted by SAK (Member # 7387) on :
Thanks so much everyone. I've tested for m. pneumoniae through my dr. There are tests at the regular lab I guess.
So, I guess I should test with Igenex PCR to be sure. All I know is that I'm still positive with these tests right now.
It's frustrating . . . My dr told me that it was a difficult co-infection to get rid of but after all these abx, I thought something would work!
Many thanks. I appreciate! Posted by Marnie (Member # 773) on :
Edited above. Yes, mycoplasms do not have a rigid cell wall, merely a cell membrane.
Re: Bb...
``Their lipid components are unusual in that they
*** include cholesterol;
this substance has been found in only one other bacterial genus, Mycoplasma.
The nutritional requirements of the borreliae are more complex than those of leptospires. Glucose, amino acids, long-chain fatty acids, N-acetylglucosamine, and several vitamins are some of their required organic nutrients.
The borreliae are microaerophilic organisms. Borrelia hermsii has a generation time of 12 hours when cultivated in artificial media at 35�C compared with only 6 to 10 hours in the mouse.''
Mycoplasmas are the only prokaryotes to date known to incorporate cholesterol or related sterols from hosts or environments to stabilize the cytoplasmic membrane, while they lack genes to synthesize or modify sterols.
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