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Some information on the step bacteria and its virulence. The most important point below is the bacteria is chemically similar to that of the host connective tissue and allow for the bacteria to hide its own antigen. Once the bad antibodies are present and the underlying bacteria is there you've got a very bad formula for continued illness.

 

-Wendy

 

 

 

The cell surface of Streptococcus pyogenes accounts for many of the bacterium’s determinants of virulence, especially those concerned with colonization and evasion of phagocytosis and host immune responses. Cell surface components include capsular polysaccharide, peptidoglycan and lipoteichoic acids, and certain membrane proteins, in addition to several structural proteins (Figure 2).

 

In Group A streptococci, the R and T proteins are used as epidemiologic markers and have no known role in virulence. The M proteins are clearly virulence factors associated with both colonization and resistance to phagocytosis. More than 50 types of S. pyogenes M proteins have been identified on the basis of antigenic specificity, and it is the M protein that is the major cause of antigenic shift and antigenic drift in the Group A streptococci. The streptococcal M protein, peptidoglycan, N-acetylglucosamine, and group-specific carbohydrate portions of the cell surface all have antigenic epitopes that mimic those of mammalian muscle and connective tissue. The cell surface of recently emerging (³flesh-eating²) strains of streptococci is distinctly mucoid (indicating that they are highly encapsulated) and rich in M protein. Protein F, thought involved in attachment to fibronectin, is presumably a nonfimbrial adhesin located on the bacterial cell surface.

 

The capsule of S. pyogenes is non antigenic since it is composed of hyaluronic acid, which is chemically similar to that of host connective tissue. This allows the bacterium to hide its own antigens and to go unrecognized as antigenic by its host The cytoplasmic membrane of S. pyogenes contains some antigens similar to those of human cardiac, skeletal, and smooth muscle, heart valve fibroblasts, and neuronal tissues, resulting in molecular mimicry and a tolerant or suppressed immune response by the host.

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Faith, Hopefully I can add some clarity with regards to number of treatments. Many immunologist believe you have to treat until the child is symptomless with IVIG. Dr. K happens to feel the larger dose is more important to shut down the bone marrow and start producing new antigens. For some kids, at the higher dose it has been one treatment, for our son its been three treatments 'so far' every eight weeks, for my friends son it has only been one treatment 'so far' and he was really, really, really, sick. It is my understanding that with a primarily TIC presentation (which was our case).... the TICs are more difficult to eradicate so often more than one treatment is required.

 

For our son, our first TIC was a cough (we had this off and on for a year prior to sudden on-set). As he recovers the coughing has been the last to resolve, we think its gone but we won't know for sure until he is further out from his last treatment. We do have an occasional flair of eye blinking now and chapped lips that come and go. Dr. K was uncertain that the last treatment was required but we have seen rapid improvement again and pray every night it holds.

 

If I had my dream treatment considering no additional risk, cost, solid immune system and our son's presentation: I would have done plasma exchange followed by a large dose of IVIG a couple weeks later and continue that until symptomless. If I was doing IVIG only, I would do the larger dose IVIG until child is symptomless. The length in between each treatment is up for debate and you really have to wait and see how the child does...... that is very painful for the parent.

 

Unfortunately, there is no standard way to treat at this point in time. I still think its going to take a few more years to figure how and when to do what. The most important thing when choosing a Dr. to treat PANDAs is having somebody that is knowledgeable (or advising) and committed to seeing success for your child given their length of illnesses, presentation and state of underlying immune system. Oops, I forgot to mention additional exposures as another variable while being treated!!!! All family members need to be check for strep or the problem will continue with re-exposures.

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Meg's Mom,

 

Are you using Augmentin and refering to the Clavulinic acid as the successful antiinflammatory? Confused? :huh:

 

 

 

Edit - ok, it took me a few hours to get this posted while working :) (who me?) and I see that you have answered this. Thanks!

 

Hey Alex - can I ask about the comment from Dr. K - because that is something that I worry about a lot, and yet struggle to justify. I am referring to the "no cure without IVIG". We have clinical diagnosis of PANDAS, classic signs, but no positive ASO/strep, onset with ear infection each time, positive CamKinII, high ANA that goes down with antibiotic treatment. Almost subclinical on Pred Burst, subclinical with antibiotics (Azith). 2 Mild episode completely treated with Azith increase (one for 8 days, as I waited for 3 days, then next for only 2 days, as I treated IMMEDIATELY as the mom suspected strep coincidental to very mild uptick in compulsions). We are only 5 months in remission.

 

So, I can't see justifying IVIG when we are at 99% - and we don't qualify for insurance (at this point) as there are no underlying immunilogical challenges that we can find. And yet are we giving her the best possible chance - always the question. We are frankly very afraid of taking her off antibiotics. We are currently doing daily tracking to see if the mild episode trend is related to the amount of Azith she is taking, as I suspect it is. If so, that would seem to indicate that we are treating her with anti-inflamatories. I hesitate to post about this, as it is completely just a suspicion on my part at this point. We are debating the correct amount for her - if preventative only, then her low dose is right. If treating something, then she needs more - and then I would have a different thought process about IVIG and the investment needed. It's a hard thing to test without taking her off - I am just not willing to do that! So we are probably 3 months out from proving a point...

 

If I understand correctly, he would say that IVIG is still needed, right? Do you understand about his basis for thinking this? Thanks SO much for posting!

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Congratulations Wendy! You've earned your honorary degree of "nerdyness"! :huh:

 

Lot's of good information, (now that my brain hurts just from trying to absorb it all)! :)

 

THANKS!

 

Lynn

 

Some information on the step bacteria and its virulence. The most important point below is the bacteria is chemically similar to that of the host connective tissue and allow for the bacteria to hide its own antigen. Once the bad antibodies are present and the underlying bacteria is there you've got a very bad formula for continued illness.

 

-Wendy

 

 

 

The cell surface of Streptococcus pyogenes accounts for many of the bacterium’s determinants of virulence, especially those concerned with colonization and evasion of phagocytosis and host immune responses. Cell surface components include capsular polysaccharide, peptidoglycan and lipoteichoic acids, and certain membrane proteins, in addition to several structural proteins (Figure 2).

 

In Group A streptococci, the R and T proteins are used as epidemiologic markers and have no known role in virulence. The M proteins are clearly virulence factors associated with both colonization and resistance to phagocytosis. More than 50 types of S. pyogenes M proteins have been identified on the basis of antigenic specificity, and it is the M protein that is the major cause of antigenic shift and antigenic drift in the Group A streptococci. The streptococcal M protein, peptidoglycan, N-acetylglucosamine, and group-specific carbohydrate portions of the cell surface all have antigenic epitopes that mimic those of mammalian muscle and connective tissue. The cell surface of recently emerging (³flesh-eating²) strains of streptococci is distinctly mucoid (indicating that they are highly encapsulated) and rich in M protein. Protein F, thought involved in attachment to fibronectin, is presumably a nonfimbrial adhesin located on the bacterial cell surface.

 

The capsule of S. pyogenes is non antigenic since it is composed of hyaluronic acid, which is chemically similar to that of host connective tissue. This allows the bacterium to hide its own antigens and to go unrecognized as antigenic by its host The cytoplasmic membrane of S. pyogenes contains some antigens similar to those of human cardiac, skeletal, and smooth muscle, heart valve fibroblasts, and neuronal tissues, resulting in molecular mimicry and a tolerant or suppressed immune response by the host.

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I am a little confused about IVIG treatments as well. I get the fact that the high dose is done to temporarily shut down the bone marrow - "re-booting" the child's immune system so to speak which makes perfect sense. However, I thought that our immune systems keep a sort of "memory bank" of all of our antibodies (even after PEX and IVIG). I understood this to mean that we would always have a "copy" of all antibodies - both good and bad - that could be called upon when needed (or in cases of autoimmune illnesses - not needed at all!!).

 

I thought this was why we didn't need to be re-vaccinated (for things like MMR etc.) even after PEX or IVIG because we should still have "copies" of those antibodies. If we keep "copies" of all of those good antibodies then why wouldn't we also keep "copies" of the bad antibodies?? Couldn't those bad antibody "copies" simply get called upon when the body thinks it needs them and then the body will manufacture more new bad antibodies (just like the the body would do if it suddenly encountered measles and it had been vaccinated against MMR (for example) before it had IVIG or PEX - the body would then find a copy of the antibody it needed to fight measles - manufacture more of the antibodies and fight the illness (in theory of course)??

 

As you can see my background is not in science!! This does kind of confuse me about PEX and IVIG though (the wheels were spinning around last night)!! I just don't get how IVIG and PEX can successfully separate the good from the bad antibodies. If anyone thinks they can help explain it I would really appreciate it!! Maybe even someone who sees Dr. K could ask him a little about it (If he is open to these types of discussions.)??

 

Thanks

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I am a little confused about IVIG treatments as well. I get the fact that the high dose is done to temporarily shut down the bone marrow - "re-booting" the child's immune system so to speak which makes perfect sense. However, I thought that our immune systems keep a sort of "memory bank" of all of our antibodies (even after PEX and IVIG). I understood this to mean that we would always have a "copy" of all antibodies - both good and bad - that could be called upon when needed (or in cases of autoimmune illnesses - not needed at all!!).

 

I thought this was why we didn't need to be re-vaccinated (for things like MMR etc.) even after PEX or IVIG because we should still have "copies" of those antibodies. If we keep "copies" of all of those good antibodies then why wouldn't we also keep "copies" of the bad antibodies?? Couldn't those bad antibody "copies" simply get called upon when the body thinks it needs them and then the body will manufacture more new bad antibodies (just like the the body would do if it suddenly encountered measles and it had been vaccinated against MMR (for example) before it had IVIG or PEX - the body would then find a copy of the antibody it needed to fight measles - manufacture more of the antibodies and fight the illness (in theory of course)??

 

As you can see my background is not in science!! This does kind of confuse me about PEX and IVIG though (the wheels were spinning around last night)!! I just don't get how IVIG and PEX can successfully separate the good from the bad antibodies. If anyone thinks they can help explain it I would really appreciate it!! Maybe even someone who sees Dr. K could ask him a little about it (If he is open to these types of discussions.)??

 

Thanks

Well, there is another, regulatory component to the immune system that is supposed to monitor for and "take out" the bad antibodies. Perhaps that's the thing PEX & IVIG fixes? We talked to the immunologist on Tuesday about IVIG...mostly it seems they don't know why it works- or at least he doesn't. I get the feeling though that he's not terribly up to date on research.

 

What I don't understand, is why our immune system doesn't make antibodies to the donor IgG, since it is nonself.

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These are great questions. I am struggling to understand this myself. Does the IVIG trick the immune system in some way so that after shutting down antibody production, it forgets to make bad antibodies but retains memory of how to fight off illness with the good antibodies? We hope to be starting monthly IVIG with Dr. B some time this month, and I want to understand if the dose of 1 gm. per kilo one day per month will work or if we are going to need to build to the higher dose that Dr. K uses.

 

Ellen

 

I am a little confused about IVIG treatments as well. I get the fact that the high dose is done to temporarily shut down the bone marrow - "re-booting" the child's immune system so to speak which makes perfect sense. However, I thought that our immune systems keep a sort of "memory bank" of all of our antibodies (even after PEX and IVIG). I understood this to mean that we would always have a "copy" of all antibodies - both good and bad - that could be called upon when needed (or in cases of autoimmune illnesses - not needed at all!!).

 

I thought this was why we didn't need to be re-vaccinated (for things like MMR etc.) even after PEX or IVIG because we should still have "copies" of those antibodies. If we keep "copies" of all of those good antibodies then why wouldn't we also keep "copies" of the bad antibodies?? Couldn't those bad antibody "copies" simply get called upon when the body thinks it needs them and then the body will manufacture more new bad antibodies (just like the the body would do if it suddenly encountered measles and it had been vaccinated against MMR (for example) before it had IVIG or PEX - the body would then find a copy of the antibody it needed to fight measles - manufacture more of the antibodies and fight the illness (in theory of course)??

 

As you can see my background is not in science!! This does kind of confuse me about PEX and IVIG though (the wheels were spinning around last night)!! I just don't get how IVIG and PEX can successfully separate the good from the bad antibodies. If anyone thinks they can help explain it I would really appreciate it!! Maybe even someone who sees Dr. K could ask him a little about it (If he is open to these types of discussions.)??

 

Thanks

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I am not sure, even the Dr.'s know the answer to this question. I could be wrong.... maybe they do.

 

If you were to look at something like Kawasaki's, they know how to diagnose, they have had great success with most children treating with a one time dose of .750 of IVIG within first couple of days of on-set of high fever. Sometimes children need more than one treatment within 48 hours of each treatment. BUT, because they found out what works in treating, most Dr.'s stopped looking for the cause of the disease. Often diagnoses is missed because it presents differently and factors involved are age of child, immune system, etc.

 

Our younger son who had Kawasaki's after being exposed to RF most likely needed more than one treatment of IVIG and why we are most likely having a PANDAS problem now. Unfortunately, we might not get all the answer and have to keep looking at what is working. Some think that IVIG also works as an anti-toxin to the exotoxin of the bacteria.

 

It is my understanding that many Dr.'s currently treating are trying to agree more formally on IVIG dose, treatment times, number, etc.

 

 

 

I am a little confused about IVIG treatments as well. I get the fact that the high dose is done to temporarily shut down the bone marrow - "re-booting" the child's immune system so to speak which makes perfect sense. However, I thought that our immune systems keep a sort of "memory bank" of all of our antibodies (even after PEX and IVIG). I understood this to mean that we would always have a "copy" of all antibodies - both good and bad - that could be called upon when needed (or in cases of autoimmune illnesses - not needed at all!!).

 

I thought this was why we didn't need to be re-vaccinated (for things like MMR etc.) even after PEX or IVIG because we should still have "copies" of those antibodies. If we keep "copies" of all of those good antibodies then why wouldn't we also keep "copies" of the bad antibodies?? Couldn't those bad antibody "copies" simply get called upon when the body thinks it needs them and then the body will manufacture more new bad antibodies (just like the the body would do if it suddenly encountered measles and it had been vaccinated against MMR (for example) before it had IVIG or PEX - the body would then find a copy of the antibody it needed to fight measles - manufacture more of the antibodies and fight the illness (in theory of course)??

 

As you can see my background is not in science!! This does kind of confuse me about PEX and IVIG though (the wheels were spinning around last night)!! I just don't get how IVIG and PEX can successfully separate the good from the bad antibodies. If anyone thinks they can help explain it I would really appreciate it!! Maybe even someone who sees Dr. K could ask him a little about it (If he is open to these types of discussions.)??

 

Thanks

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