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I'm no expert, but my understanding is that PANDAS is just one subtype of a broader category of post-infectious autoimmune disorders called PITAND (Pediatric Infection-Triggered Autoimmune Neuropsychiatric Disorders). I believe that researchers originally coined the term PITAND for the broader spectrum of these types of illnesses, acknowledging that many viral and bacterial triggers caused a similar set of symptoms. PANDAS identified the subgroup of patients who seemed to clearly and consistently react to GABHS infections... although even these patients exacerbated when exposed to non-strep infections after the initial strep autoimmune reaction was initiated.

 

So PITAND is the superset, I think, and PANDAS is the subset. Many parents on here have kids who are PITAND but not PANDAS, which is why the nice folks at ACN who host this forum changed the name to "PANDAS and PITAND" a while back. And of course, Lyme / co-infections factor into this as well, even though there's still uncertainty about whether they involve an autoimmune response.

 

Sigh. It's all pretty darned confusing, isn't it?

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To add more confusion, it seems some of these kids start as soley PANDAS and then become PITAND as they begin to not only react to strep. Then you have other kids, like my son, that started as strep only (PANDAS), started to react to other things (PITAND), now doesn't react to non-strep triggers, but I assume (and hope I never find out) he will still react to strep itself. Confusing enough? :blink:

 

There's also a history of PANDAS section in the pinned threads you might find interesting. http://www.latitudes.org/forums/index.php?showtopic=5144&st=0&p=36300entry36300Here's a small part of it...

 

ARF and the D8/17 marker

 

In 1989 Swedo published her study looking at 70 children with OCD over a ten year period where she noted the incredible similarity in symptoms.

By 1993, Bronze and Dale published their findings that neural tissue had cross reactivity with antibodies to the M protein from strep emm-type 6. This was essentially a rediscovery of Husby but with the further isolation that the antibodies were to the M protein.

In 1994, Swedo published a fascinating paper entitled “Speculations on antineuronal antibody-mediated neuropsychiatric disorders of childhood” where she proposed the hypothesis that neurological abnormalities of childhood may be caused by antineuronal antibodies resulting from a GABHS infection. This seemed to combine Husby’s, Bronze, Dale theories together.

In 1995, Swedo and Allen found 4 children who exhibited sudden onset OCD symptoms coincident with infections. Two of the children had exacerbations coincident with GABHS infections and two with viral infections. Treatment with plasmapherisis, IVIG and prednisone were all found effective. They called this treatable subset of OCD, PITAND (pediatric infection-triggered auto-immune neuropsychiatric disorder).

In 1997, Swedo found that the D8/17 marker from Khanna (1989) work on Acute Rheumatic Fever seemed to correlate and support the theory of a distinct genetic pre-disposition for OCD and chorea. She labeled this distinct OCD subgroup PANDAS – in case you wondered where the term came in.

Edited by Vickie

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I wonder why, then, all the studies seem to be aimed at PANDAS---the strep connection?? It seems like if you can't link symptoms to strep, you are sort of in the "hmmmm...." category. Also, to me, this explains why antibiotics are not helping my daughter at this point in the game.

 

edit: and if this is the case, PITAND...what do you do???

Edited by eljomom

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My son has normal strep titers. They show absolutely no evidence of strep. He's never had a throat culture done. Strep was never suspected. He's rarely sick. He has not had a known illness since Feb 2010, when he had an ear infection. No runny nose, cough, fever, sore throat, vomiting, etc..... His PANDAS, if you want to call it that, started up after the Flu Mist in fall 09. I just got his Cunningham results back today. His Cam Kinase II is 144, that's in the low PANDAS range. His anti-tubulin is high. Sixty days of biaxin has brought him back to about 95%. He's been on prophylactic zithro 2x week for a month now and holding his own. It would seem that a child w/ normal strep titers and normal myco titers and a viral trigger would not improve w/ antibiotics, but he has. I have no explanation.

 

Cindy

Edited by nicklemama

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I wonder why, then, all the studies seem to be aimed at PANDAS---the strep connection?? It seems like if you can't link symptoms to strep, you are sort of in the "hmmmm...." category. Also, to me, this explains why antibiotics are not helping my daughter at this point in the game.

 

edit: and if this is the case, PITAND...what do you do???

 

I think the answer to that is because this is where Dr. Susan Swedo at the NIMH started . . . with strep. And considering the struggles she's had having her strep studies validated, further diversifying her research into other triggers is probably not an option . . . at least not yet. She does acknowledge in her speeches, however, that there are other auto-immune triggers.

 

Meanwhile, it's my understanding that while Dr. Madeliene Cunningham's current field of study is limited to the SC/PANDAS realm, some of the neurotransmitter marker levels her research is identifying are being related to other conditions, and she has met with other doctors regarding the PITANDS pieces of the puzzles such as myco p and Lyme.

 

It's all a matter of time and funding, it would appear.

 

As for antibiotics not helping your child, have you tried different antibiotics? Sorry . . . I can't retain the histories of all the families here. Just wondering if it's possible that your child would respond to a different class of medication than you've had the opportunity to try thus far?

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My son has normal strep titers. They show absolutely no evidence of strep. He's never had a throat culture done. Strep was never suspected. He's rarely sick. He has not had a known illness since Feb 2010, when he had an ear infection. No runny nose, cough, fever, sore throat, vomiting, etc..... His PANDAS, if you want to call it that, started up after the Flu Mist in fall 09. I just got his Cunningham results back today. His Cam Kinase II is 144, that's in the low PANDAS range. His anti-tubulin is high. Sixty days of biaxin has brought him back to about 95%. He's been on prophylactic zithro 2x week for a month now and holding his own. It would seem that a child w/ normal strep titers and normal myco titers and a viral trigger would not improve w/ antibiotics, but he has. I have no explanation.

 

Cindy

I wonder if he would have cultured positive for strep before abx. Because, except for the flu mist, that describes my daughter to a T. She was never tested for strep until she was ten...and didn't have symptoms then, but tested positive every time she was off abx for 3-5 days.

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I wonder if he would have cultured positive for strep before abx.

 

I have wondered the same. It is possible the Flu Mist was a red herring that just happened to be given when he was brewing strep or it made things worse than they might have been.

 

I doubted myself many, many times while pursuing PANDAS for my DS7. It kept me from being more aggressive and letting it go on for so long. He's always been so healthy and rarely sick. However, looking at his sudden onset and symptoms, he was classic for PANDAS, if you can overlook the lack of confirmed strep. My friend's kids were/are sick all the time. Its always something....coughing, runny nose, fever, etc... My son would not get sick even w/ exposure to their sick kids. The jokes on me since he has turned out to be the "sickest" one of them all.

 

Cindy

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ugh---just posted a long reply to you nicklemama, but in a nutshell i can relate to the joke being on me. I ran my first 3 kids to the doctor every fever, strep, ear infxn, and antibiotics so much they each developed an allergy to certain abx....then my 4th (panda-child), sick all the time too, abx a ton, then finally decided to let things run their course. so stopped taking to doctor---for a few years, only for well-checks. fevers, sore throats, etc....motrin and time...and she always got well......or so I thought. now this---i have so many regrets from this, and now I am living in fear of making another mistake and messing her up more.

 

I wonder if he would have cultured positive for strep before abx.

 

I have wondered the same. It is possible the Flu Mist was a red herring that just happened to be given when he was brewing strep or it made things worse than they might have been.

 

I doubted myself many, many times while pursuing PANDAS for my DS7. It kept me from being more aggressive and letting it go on for so long. He's always been so healthy and rarely sick. However, looking at his sudden onset and symptoms, he was classic for PANDAS, if you can overlook the lack of confirmed strep. My friend's kids were/are sick all the time. Its always something....coughing, runny nose, fever, etc... My son would not get sick even w/ exposure to their sick kids. The jokes on me since he has turned out to be the "sickest" one of them all.

 

Cindy

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I wonder why, then, all the studies seem to be aimed at PANDAS---the strep connection?? It seems like if you can't link symptoms to strep, you are sort of in the "hmmmm...." category.

 

Hi Eljomom,

 

I absolutely get your question. The reason all the studies were on strep is that Swedo was looking at sudden onset OCD in kids who developed sydenham chorea. Sydenham Chorea is generally accepted as a sequela to untreated GABHS infection. She noticed that sometimes the OCD came before the chorea and sometimes after.

 

She then got some kids with sudden onset OCD but didn't get chorea. That's weird (she thought). Is the sudden onset OCD something else?

 

About 21% of patients who get Acute Rheumatic Fever gets sudden onset OCD. About 30% of patients with Acute Rheumatic Fever get Sydenham Chorea, but only 70% of those who get SC get OCD and apparently a few kids (i.e., the 50 she was looking at) get OCD but no SC.

 

So now she's thinking -- I wonder if the SC and OCD are triggered by the same antibody or is it two different antibodies.

 

She found in a really small study that two kids with sudden OCD but no SC had strep and another two kids with sudden OC but no SC had a virus.

 

So now she's stuck. It could be that it's caused by strep or caused by a virus. She tried immunomodulating therapy and all the kids got better. Now that's weird (she thought again).

 

Others tried treating the OCD in SC kids with IVIG and they got better too. Wow! Another group tried treating OCD in non-SC kids and they didn't get better at all. Hmmm, somethings going on here. Maybe this sudden onset is the thing.

 

She's got a bunch of people around her who know tons about streptococcus so she focuses there first. Here's the key -- it's possible sydenham chorea might also be streptococcus and viruses too... Everyone sort of thinks it only comes from untreated strep -- but maybe not.

 

So the team starts looking at just untreated streptococcus -- she thought this would be easy to prove, then they could come back to those pesky viruses. But now here's the key problem she ran into....

 

In her original definition, she said that PANDAS was sudden and dramatic onset of OCD and/or tics. Kurlan flipped out and said "all tics are dramatic and sudden". So Swedo's stuck -- how does she look for these auto-antibodies if she doesn't have a good way to separate out the kids who have them from the kids who don't.

 

Swedo landed on these comorbid or coincident psychological manifestations. The kids who seeemed to fit this PANDAS profile had separation anxiety and daytime urinary frequency and other such symptoms. So Kirvan and Cunninham used serum from a group of kids who had OCD and these other symptoms and started looking for the preverbial needle in haystack and found antibody 24.3.1.

 

Now the question is whether the kids with just tics caused by auto-immune have this 24.3.1. We frankly don't know. Kurlan sort of refused to pursue any kids with the dramatic onset of OCD (i.e., he stuck to kids with long term tics) and kept not finding the anti-basal ganglia antibodies. Most likely because he didn't actually have any kids who fit the expanded PANDAS profile (i.e., the ones with seperation anxiety or daytime urinary frequency or dilated pupils, ...).

 

So I totally get what you are saying that "what happened to all the folks who are affected primarily by non-strep" -- right now Swedo still doesn't have everyone agreeing that 24.3.1 (cunningham's tests) are meaningful. So she's still working that one and until she can prove that, there's not a lot of money/research being spent on other harder to find viruses and bacteria.

 

Buster

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Wow Buster---your explanation is what I have been looking for! Thank you for taking the time to put all that out there. I have actually been thinking about calling Swedo, but doubt she would talk "off the cuff" and give me the real deal.

 

So this antibody 24.3.1---is that what the Cam K is responding to? Can you explain how they are testing that specifically? Sorry---I'm a "need to understand" person...and I am lying awake at night trying to figure this all out. I keep thinking I understand the Cam K, but then I realize I really don't. Is it elevated from inflammation, from the antibody, or from an autoimmune response? Since my daughters symptoms started suddenly, and have not remitted, then does that mean the "cause" is still lurking (which in my heart I truly, truly doubt), or that the autoimmune process was set off, and is still causing symptoms? Can an autoimmune illness cause symptoms even when there are no bateria/viruses going on? This is what I don't get....

 

Thanks again for your patient responses, Buster.

 

I wonder why, then, all the studies seem to be aimed at PANDAS---the strep connection?? It seems like if you can't link symptoms to strep, you are sort of in the "hmmmm...." category.

 

Hi Eljomom,

 

I absolutely get your question. The reason all the studies were on strep is that Swedo was looking at sudden onset OCD in kids who developed sydenham chorea. Sydenham Chorea is generally accepted as a sequela to untreated GABHS infection. She noticed that sometimes the OCD came before the chorea and sometimes after.

 

She then got some kids with sudden onset OCD but didn't get chorea. That's weird (she thought). Is the sudden onset OCD something else?

 

About 21% of patients who get Acute Rheumatic Fever gets sudden onset OCD. About 30% of patients with Acute Rheumatic Fever get Sydenham Chorea, but only 70% of those who get SC get OCD and apparently a few kids (i.e., the 50 she was looking at) get OCD but no SC.

 

So now she's thinking -- I wonder if the SC and OCD are triggered by the same antibody or is it two different antibodies.

 

She found in a really small study that two kids with sudden OCD but no SC had strep and another two kids with sudden OC but no SC had a virus.

 

So now she's stuck. It could be that it's caused by strep or caused by a virus. She tried immunomodulating therapy and all the kids got better. Now that's weird (she thought again).

 

Others tried treating the OCD in SC kids with IVIG and they got better too. Wow! Another group tried treating OCD in non-SC kids and they didn't get better at all. Hmmm, somethings going on here. Maybe this sudden onset is the thing.

 

She's got a bunch of people around her who know tons about streptococcus so she focuses there first. Here's the key -- it's possible sydenham chorea might also be streptococcus and viruses too... Everyone sort of thinks it only comes from untreated strep -- but maybe not.

 

So the team starts looking at just untreated streptococcus -- she thought this would be easy to prove, then they could come back to those pesky viruses. But now here's the key problem she ran into....

 

In her original definition, she said that PANDAS was sudden and dramatic onset of OCD and/or tics. Kurlan flipped out and said "all tics are dramatic and sudden". So Swedo's stuck -- how does she look for these auto-antibodies if she doesn't have a good way to separate out the kids who have them from the kids who don't.

 

Swedo landed on these comorbid or coincident psychological manifestations. The kids who seeemed to fit this PANDAS profile had separation anxiety and daytime urinary frequency and other such symptoms. So Kirvan and Cunninham used serum from a group of kids who had OCD and these other symptoms and started looking for the preverbial needle in haystack and found antibody 24.3.1.

 

Now the question is whether the kids with just tics caused by auto-immune have this 24.3.1. We frankly don't know. Kurlan sort of refused to pursue any kids with the dramatic onset of OCD (i.e., he stuck to kids with long term tics) and kept not finding the anti-basal ganglia antibodies. Most likely because he didn't actually have any kids who fit the expanded PANDAS profile (i.e., the ones with seperation anxiety or daytime urinary frequency or dilated pupils, ...).

 

So I totally get what you are saying that "what happened to all the folks who are affected primarily by non-strep" -- right now Swedo still doesn't have everyone agreeing that 24.3.1 (cunningham's tests) are meaningful. So she's still working that one and until she can prove that, there's not a lot of money/research being spent on other harder to find viruses and bacteria.

 

Buster

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So this antibody 24.3.1---is that what the Cam K is responding to?

 

It sure looks like at least 24.3.1 is causing Cam Kinase II activation. There may be a couple other antibodies that are doing it too, but 24.3.1 seemed to be both an anti-lysoganglioside (discussed in a moment) and a CaM Kinase II activator.

 

Can you explain how they are testing that specifically?

 

Yikes. Well, let me try an explanation here and we'll see if it help. CaM Kinase II activation is generally tested by assay or microplate. A sample of blood serum (which contains antibodies) is incubated with neuronal tissues (typically those from neuroblastoma cells) to generate a potential CaM Kinase II sample. The sample is then incubated with a microplate substrate in the presence of a radioactively tagged ATP. Consider this a radioactive flag that signals that a particular type of activation is occuring. There's a bunch of steps next that wash the substrate, but the end result is that the microplate will have a radio-signature that indicates a quantity of CaM Kinase II activation.

 

While in the Nature paper, Kirvan isolated and cloned the 24.3.1 antibody. These days I think they test without isolating the individual antibody, but rather taking a diluted sample of blood serum and seeing if any of the ATP changes state (i.. raises the flag). If it does then they assume the likely cause is the 24.3.1 antibody. It's a pretty good bet.

 

Now CaM Kinase II regulates Calcium channels and potentiation (meaning keeping channels open). This has effect on cell signalling (particularly fo neurons). So lots of CaM Kinase II activation likely means a lot of neurons would be firing.

 

microplate_activity_diagram.jpg

 

Is Cam Kinase elevated from inflammation, from the antibody, or from an autoimmune response?

 

It appears it is elevated from a specific antibody (which is an autoimmune response).

 

Can an autoimmune illness cause symptoms even when there are no bateria/viruses going on? This is what I don't get....

Absolutely. Here's the way to think about it. When you get an infection, your body produces antibodies to help find bacteria and flag it. Quite literally antibodies are little Y shaped structures that attach to specific carbohydrates or proteins on a cell surface. They flag for destruction. There's these other cells known as macrophages that come along and see the flag and "eat" the bacteria. The macrophages then send a signal saying "found some" or "make more antibodies" (this is a short hand, there's a lot going on here). Anyway, the body makes more antibodies and more macrophages until the infection is resolved.

 

Now when the infection is gone, the anti-bodies will still be around for a while (typically 21-28 days). This is actually a half-life. This means every 21 days about half the antibodies have been used up. Now this assumes you don't get another infection that ramps everything back up.

 

In auto-immune diseases, a portion of the host can act as a recipient of the Y antibody. This is a mistake (i.e., the immune system is supposed to not make antibodies that will bind with host cells. For whatever reason the check of "is it going to attack the host" is broken or ineffective so the feedback cycle starts. The target of the auto-immune disease (think neuron cells) now acts as if it were the bacteria. The immune system sees these monoclonal antibodies and tries to engulf the cell.

 

Do we know that this is what is really going on.... not really, but it sure seems plausible.

 

You could therefore ask how do you break the cycle? Well if the stuff is across the blood brain barrier, closing the BBB helps break the cycle. If the stuff is heart muscle or joints or ... then prednisone can help break an autoimmne cycle.

 

It is not known whether the antibiotics are having an immunomodulating effect, an antiinflammatory effect and closing the BBB, or some other effect.

 

Please post again if above isn't clear.

 

Buster

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OK Buster---I think I"m getting closer to the a-ha moment! You are really clarifying many things for me. So, let me make sure I am uderstanding if you don't mind: it seems there are really 2 more distinct types of pandas/pitand kids here---1 type that responds to antibiotics because it shuts down the bacteria, and the antibodies eventually die out, and the exacerbation resides. Then there is the second kid (mine) who continues to have symptoms even after the bacteria/virus is gone because now the antibodies are going after self-tissue (in the basal ganglia)....and at this point, antibiotics are not going to be as helpful (other than the POSSIBILITY of them helping with inflammation,etc...)??? If so, this should guide the course of treatment, right? Also, the Cam K being high in "normal kids" with active strep might be saying that Cam K scores are more relevant to Kid #1 described above, and once infection clears, and antibodies die off, all is good in the world. And that anti-neuronals might then be a better tool for the kids who continue to have symptoms beyond the normal "antibiotic clears illness---antibodies die off" because these auto-antibodies indicate that there is truly AUTO-IMMUNE (hence ANTI-DOPAMINE, etc.. ANTIBODIES) problem going on???

 

So the million dollar question then is: What do do if your kid falls into #2?? You mentioned steroids helping if the problem is outside the BBB, but if it's across the BBB---do steroids help close it? Or do you go straight to IVIG---does that help close it?

 

And the 2 million dollar question is: do you take these extreme measures if your kid is still functioning? Ticcing like CRAZY, ocd is not non-functional, hyper, sep. anxiety are tolerable b/c we homeschool....what then. It's so hard to do nothing when you know what is likely happening. Why wait for it to get horrible, and why not do something if you can? Which leads me to the 3 million dollar question---does IVIG really work and "cure"? And I really haven't looked into the possible negative-impacts of these things yet, but is it worth risking those things and making things even worse....these are the decisions I lie awake at night pondering....

So this antibody 24.3.1---is that what the Cam K is responding to?

 

It sure looks like at least 24.3.1 is causing Cam Kinase II activation. There may be a couple other antibodies that are doing it too, but 24.3.1 seemed to be both an anti-lysoganglioside (discussed in a moment) and a CaM Kinase II activator.

 

Can you explain how they are testing that specifically?

 

Yikes. Well, let me try an explanation here and we'll see if it help. CaM Kinase II activation is generally tested by assay or microplate. A sample of blood serum (which contains antibodies) is incubated with neuronal tissues (typically those from neuroblastoma cells) to generate a potential CaM Kinase II sample. The sample is then incubated with a microplate substrate in the presence of a radioactively tagged ATP. Consider this a radioactive flag that signals that a particular type of activation is occuring. There's a bunch of steps next that wash the substrate, but the end result is that the microplate will have a radio-signature that indicates a quantity of CaM Kinase II activation.

 

While in the Nature paper, Kirvan isolated and cloned the 24.3.1 antibody. These days I think they test without isolating the individual antibody, but rather taking a diluted sample of blood serum and seeing if any of the ATP changes state (i.. raises the flag). If it does then they assume the likely cause is the 24.3.1 antibody. It's a pretty good bet.

 

Now CaM Kinase II regulates Calcium channels and potentiation (meaning keeping channels open). This has effect on cell signalling (particularly fo neurons). So lots of CaM Kinase II activation likely means a lot of neurons would be firing.

 

microplate_activity_diagram.jpg

 

Is Cam Kinase elevated from inflammation, from the antibody, or from an autoimmune response?

 

It appears it is elevated from a specific antibody (which is an autoimmune response).

 

Can an autoimmune illness cause symptoms even when there are no bateria/viruses going on? This is what I don't get....

Absolutely. Here's the way to think about it. When you get an infection, your body produces antibodies to help find bacteria and flag it. Quite literally antibodies are little Y shaped structures that attach to specific carbohydrates or proteins on a cell surface. They flag for destruction. There's these other cells known as macrophages that come along and see the flag and "eat" the bacteria. The macrophages then send a signal saying "found some" or "make more antibodies" (this is a short hand, there's a lot going on here). Anyway, the body makes more antibodies and more macrophages until the infection is resolved.

 

Now when the infection is gone, the anti-bodies will still be around for a while (typically 21-28 days). This is actually a half-life. This means every 21 days about half the antibodies have been used up. Now this assumes you don't get another infection that ramps everything back up.

 

In auto-immune diseases, a portion of the host can act as a recipient of the Y antibody. This is a mistake (i.e., the immune system is supposed to not make antibodies that will bind with host cells. For whatever reason the check of "is it going to attack the host" is broken or ineffective so the feedback cycle starts. The target of the auto-immune disease (think neuron cells) now acts as if it were the bacteria. The immune system sees these monoclonal antibodies and tries to engulf the cell.

 

Do we know that this is what is really going on.... not really, but it sure seems plausible.

 

You could therefore ask how do you break the cycle? Well if the stuff is across the blood brain barrier, closing the BBB helps break the cycle. If the stuff is heart muscle or joints or ... then prednisone can help break an autoimmne cycle.

 

It is not known whether the antibiotics are having an immunomodulating effect, an antiinflammatory effect and closing the BBB, or some other effect.

 

Please post again if above isn't clear.

 

Buster

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Johnsmom, Eljomom, and Buster - thank you so much for this great thread. I don't mean to hijack it and Buster can answer on another thread if better... but I have a question too.

 

There has been some discussion recently on another thread about the strep specificity of the antibodies used in the Cunningham test. I see that in 2003 they isolated 24.3.1 but in the 2006 article they do not state it was 24.3.1. Your explanation below clarifies that.

While in the Nature paper, Kirvan isolated and cloned the 24.3.1 antibody. These days I think they test without isolating the individual antibody, but rather taking a diluted sample of blood serum and seeing if any of the ATP changes state (i.. raises the flag). If it does then they assume the likely cause is the 24.3.1 antibody. It's a pretty good bet.

 

So - here are my two questions:

1. Is 24.3.1 SPECIFIC to strep. That is - does 24.3.1 rise in the presence of antigens other than strep.

 

2. If my son's blood was run on the Cunninghma test in 2010 is it possible / plausible that the rise in Cam Kinase was due to an antibody OTHER than 24.3.1. That is - if he had some other type of infection, could that have caused the rise in Cam Kinase?

 

Thanks!

Edited by kimballot

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