Trying to understand Mycoplasm Antibodies

[inhstyme]

Hello all! 🙂
I started on AP (doxycycline) a little over 7 weeks ago for Lupus (SLE). I can’t even tell you how AMAZING I am doing on this, and SO thankful!

I am trying to understand how the mycoplasm is affected by the antibiotic. I have read up quite a bit about why the mycoplasm is a culprit in my disease and why the antibiotic works, I’m just wondering what to expect down the road with my future labs to make sure it is indeed working.

My initial lab work showed that I don’t currently have a M. pneumoniae infection (no shocker), but I did test positive for both IgG and IgM antibodies. The IgG was 2.97 and the IgM was 1.67. Is it correct to assume that in the future, after being on the antibiotic for a period of time that I will test negative for the IgG and IgM antibodies, or will they always be there?

Thanks in advance! After seeing what so many people are going through with this disease while following the mainstream treatments, I am SO grateful to already be symptom free without any side effects! 🙂

[Lynne G.SD]

Hi;
Purple panda’s post is just below your’s with links to the CPN site that should give you answers.I sort of suspect that the few weeks of AP and no symptoms is just the honeymoon phase of getting well.Don’t be surprised if the SLE comes back to hit you.AP is a very slow therapy and soooooo worth it.

[Maz]

@inhstyme wrote:

Hello all! 🙂
I started on AP (doxycycline) a little over 7 weeks ago for Lupus (SLE). I can’t even tell you how AMAZING I am doing on this, and SO thankful!

🙂

Hi inhstyme,

How wonderful that you feel you’re doing so well, so swiftly, on the therapy! 🙂 It can be a bumpy road for some – not necessarily all – so we’ll keep our fingers crossed for you that you fall into the latter category. Would you say you’ve experienced any herxing at all after beginning treatment? Can you also perhaps add a signature line that includes your diagnosis, protocol (type of abx and dosing schedule) and any other meds/supps you might be taking? A signature line will pop up each time you post as a footer and can be updated at any time, but helps others to answer any questions that you might want to ask. For E.g….for the question directly below, it would be helpful to know your dose, because if you are only treating mycoplasma, then a small, pulsed, intermittent dose is sufficient for this type of cell wall-deficient bug.

I am trying to understand how the mycoplasm is affected by the antibiotic. I have read up quite a bit about why the mycoplasm is a culprit in my disease and why the antibiotic works, I’m just wondering what to expect down the road with my future labs to make sure it is indeed working.

The tetracycline class of antibiotics (e.g. tetracycline, doxycycline and minocycline) are of the “bacteriostatic” variety. Some antibiotics, like penicillins, are bacteriocidal, which means they work by killing bugs outright by destroying their cells walls. On the other hand, some bugs, like mycoplasma, are cell wall-deficient and they only have a thin, outer lipid layer. Therefore, a penicillin type of abx would have no effect on them, which is why a bacteriostatic is used. Bacteriostatics penetrate the bug to disable it by interfering with certain processes needed for them to function and, in lower doses, do not kill the bug – the immune system will then go after the bug to kill and remove it (note: which is why folks who are being effectively immunosuppressed will usually require higher daily dosing). This is how mycoplasmas are affected by this type of antibiotic. This wiki link explains further:

http://en.wikipedia.org/wiki/Bacteriostatic_agent

If you get a chance, try to read and re-read the Henry Scammell book, The New Arthritis Breakthough to grasp the rationale for treating rheumatic disease caused specifically by mycoplasmas (there are other potential infectious offenders, too). Dr. Brown describes rheumatic disease as a bacterial “allergy” or “hypersensitivity” state, wherein the affected person’s body becomes sensitized to the toxins (antigens) released by the bugs during their regular life processes and when they die. In fact, RA and lupus are described as Type III hypersensitivity diseases in the conventional literature, so this is nothing new. Neither is “bacterial hypersensitivity,” which is a commonly accepted medical term for a patient who becomes very unwell as a result of a microbe’s antigenic substances.

http://en.wikipedia.org/wiki/Type_III_hypersensitivity

When you are asking about what to expect with your labs down the road, do you mean your mycoplasma labs and/or your lupus labs? This is quite a complex subject, but the bare essentials can be narrowed down as follows:

When testing for microbial titers via IG (immunoglobulins – e.g. IgM and IgG), this is a called “indirect” testing, meaning the test is looking for the host’s (your) response by measuring the antibodies that are being produced as a result of a particular infection. Where this gets complicated in some instances is that when the host antibodies become complexed (bound up together) with the bug antigen, the test will not provide an accurate reading. This can happen in some of the sickest patients, which is why indirect testing should not be the only parameter for testing or assuming there is lack of evidence of infection. My Lyme doc used to test my immune complexes as he felt it was a more accurate gauge, in my case, of infectious disease activity. PCR (polymerase chain reaction) testing is also used (Brown used this type of testing) and this is a direct form of testing, meaning a the lab technician will be looking for the genetic material of a bug to try to identify it in one small sample of blood. While this type of testing is highly specific (meaning if the genetic material is found, there is no doubt the bug is there), it lacks sensitivity, because it relies on the bug being detected in a small blood sample. So, no test is foolproof, in other words. I’m not sure what lab you used or the lab’s reference range for positivity, but what Brown would do is to treat until all symptoms were in remission and all labs (both disease, plus any incidentals, like anemia or leukopenia, plus infection markers) were normalized. How long this takes for each person is very individual, reliant on many variables (age, disease type and duration, co-morbidities, hormonal imbalances, lifestyle choices, etc.). His goal was to get folks off their abx eventually and, in some cases this was successful, but the majority of rheumatic patients prefer to remain on their treatments, considering them relatively benign as compared to the alternatives or the risk of relapse.

My initial lab work showed that I don’t currently have a M. pneumoniae infection (no shocker), but I did test positive for both IgG and IgM antibodies. The IgG was 2.97 and the IgM was 1.67. Is it correct to assume that in the future, after being on the antibiotic for a period of time that I will test negative for the IgG and IgM antibodies, or will they always be there?

In some instances, it can be very helpful to be able to “prove” infection, both to a less than enamored doctor or to help get IVs approved. Try to remember that probably most of the world’s population has been exposed to one type of pathogenic mycoplasma or another. It’s everywhere – in the air, food we eat, soil…it’s a very common lab contaminant. The difference for rheumatics and your average health person is like that of two people standing in a barn full of hay and one will be allergic to the hay and the other will be unphased by all the dust. The other consideration is that it’s possible to be re-infected by another passing infection, so titers may go up and down all the time and one lab reading is just a moment in time. The long-range goal is to have those microbial titers come down, but, more importantly, it is critical to get the immune system re-trained to react less violently to the bacterial antigen by slowly and carefully treating the bugs, but also assisting the immune system to re-gather its strength to hold the animals in the zoo. We never get rid of all bugs completely, for good or forevermore, nor can we remain in a bubble to prevent future re-infection, so it’s of critical import to also ensure you’re doing everything possible to re-gain health through appropriate diet and immune system supports. It can take many years of unwitting abuse to our bodies (chronic stress, poor diet leading to leaky gut, pollution, exposures to household and food chemicals, preservatives in vaccinations, lifestyle choices, overconsumption of alcohol, smoking, and even exposures in the womb, etc.) for homeostasis (balance) to be lost and then that one, or several, pesky apples (e.g. mycoplasma or Lyme) comes along and tips the proverbial apple cart.

None of this is meant to cause unnecessary concern, because you seem to be responding remarkably quickly, but just to say that while some people may get well again quite quickly, right out of the gate, just by taking their antibiotics, others may have a much harder time regaining remission. They have many nails in their feet and each nail needs to be identified and removed in order for the immune system to find balance and harmony again. A distracted immune system has a much harder time finding remission. So, I think this may be what Lynne is wisely referring to above. For many, it can be a bit of a forward and backward dance to remission, with periods of seeming remission and relapse. However, what seems pretty universal is that the flare times tend to follow a pattern in the longer term of becoming less violent, less frequent and shorter in duration until sustained remission is reached.

Thanks in advance! After seeing what so many people are going through with this disease while following the mainstream treatments, I am SO grateful to already be symptom free without any side effects!

You are fortunate to have found AP quite early in your disease. There are many others here who are using both conventional drugs and AP with the goal of reverting to AP only when they have found their disease symptoms are settling down. There are many paths to Rome, so to speak, but patient experience has repeatedly shown that the folks who find remission swiftly on AP are those who start early (Brown talks about this, too, in the book) and have fewer “nails” to remove from the soles of their feet.

Does that help, inhstyme? Everyone who has been here a while knows I go overboard with explanations, but I recall those early scary days and how simple explanations could really relieve a lot of worry. Also, quite often others are asking similar questions, so hopefully something will be of value to others who managed to remain awake to this point, as well. 😆

[inhstyme]

Thank you ladies so, SO much for all the helpful info!! I am trying to learn as much as I can about all of this. 🙂 My ND diagnosed the lupus based on my symptoms, a positive ANA titer and a positive anti-dsDNA. Prior to AP my symptoms were very mild thankfully and nothing has indicated that I have any organ involvement, so I am very fortunate to have caught it early and even more fortunate to have heard about AP even before I received my diagnosis.

I did have a mild herx about 3 days into AP where I felt nauseous, dizzy and had a pretty good headache. About 7-10 days into treatment my joint aches were virtually gone and my fatigue was remarkably improved. For the last few years exercise had left me with pain in my muscles and/or joints and they felt like they were on fire. The pain would last for at least a week and in one instance it lasted for 9 months! Last week I attempted some yard work and spent some time walking and jogging on my treadmill. I only had very mild muscle soreness that lasted 2-3 days. It’s like a miracle and I just want to shout it from the roof tops! 😀

Thank you again for taking the time to respond to my question, I genuinely appreciate it!

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