Can Lyme cause molecular mimicry?

[norcalmom]

Does anyone know Lyme raises anti-neuronal antibodies as well as cam K? Or is it only cam k if uncomplicated Lyme ?

 

I am trying to figure out if Lyme triggers the same weird antibody response as pandas (was it 24.1?) or if the fact that Lyme is present will raise cam k. I assumed that an infection with strep, Lyme, myco would set off the "pandas reaction"(molecular mimicry) and lead to a raised cam k along with anti neuronals. But I am reading some old posts and they seemed to state no, it is different, but it is unclear- that wasn't the topic if the thread.

 

Does a raised cam k alone mean an autoimmune response is taking place?

 

In which case ivig would not be necessary for lyme kids-they just need to get rid of the Lyme- it isn't an autoimmune reaction to the Lyme, like strep. Am I making sense?

[KeithandElizabeth]

Gosh, i am really driving myself crazy with these same thoughts right now. My 11 year daughter had a 179 Cam K and very high anti-neuronal levels (dopamine 1 was 4 times the normal level) and she failed 13 out of 14 S. Pneumo titers and her IGG's levels were barely normal.

 

We have been treating her for lyme disease, mycoplasma and babesia (the strep went away immediately) and she is doing great!!!!! Depending on the day, she is about 93% better, but she still has babesia. She has a scheduled IVIG in 2 1/12 weeks and I am about to reschedule it for the fifth time because I am so on the fence.

 

After doing 2 hdIVIG's and 4 or 5 small dose IVIG's with our son, we are not convinced that IVIG is the answer if lyme is the main issue. Both of our children had strep issues, but they also have other microbes so I am thinking that I will maybe redo the Cunningham and S. Pneumo titers and then go from there.....

 

In the back of my mind though, I am so worried that I may make the wrong decision.

 

Anyway, to answer your question, I do think that lyme can cause molecular mimicry.

 

Elizabeth

[kimballot]

Does anyone know Lyme raises anti-neuronal antibodies as well as cam K? Or is it only cam k if uncomplicated Lyme ?

 

I am trying to figure out if Lyme triggers the same weird antibody response as pandas (was it 24.1?) or if the fact that Lyme is present will raise cam k. I assumed that an infection with strep, Lyme, myco would set off the "pandas reaction"(molecular mimicry) and lead to a raised cam k along with anti neuronals. But I am reading some old posts and they seemed to state no, it is different, but it is unclear- that wasn't the topic if the thread.

 

Does a raised cam k alone mean an autoimmune response is taking place?

 

In which case ivig would not be necessary for lyme kids-they just need to get rid of the Lyme- it isn't an autoimmune reaction to the Lyme, like strep. Am I making sense?

 

I have also been thinking about this. On a very basic level, I would assume that lyme has the capacity to set off a PANDAS exacerbation just like any other infection has the capacity to do so. I also would think that steroids and/or IVIG would be important once the lyme is removed IF the symptoms do not subside, as that autoimmune response can self-perpetuate (antibody 24.31 continues to recognize basal ganglia cells as antigen and keeps producing antibody to attack it .... antibody attaches and increases Cam Kinase II..... Neural tissue does not go away, so body produces more antibody...etc). Steroids and IVIG shut down this autoimmune response and also reduce inflammation and seal off the blood brain barrier (from what I understand). I think that is why some folks are seeing clearer resolve of the PANDAS symptoms once lyme is treated- the base infection is gone, so the inflammation is down for long-term.

 

I believe it is also possible for the lyme spirochetes to directly affect brain tissue, but I do not think this is what is being measured in the Cunningham test. I am thinking that these direct neurological lyme characteristics can be seen in anyone - not just people with the PANDAS predisposition to an autoimmune disorder.

 

Does that make sense???

[justinekno]

Maybe this is a question worth emailing to Dr. Cunningham? I know she has had some emails from some of us on the Forum asking about the relation of Lyme and CamKinase. Maybe if she doesn't know the answer, she could include it with the other Lyme info she is looking into (one being congenital Lyme).

 

Does anyone know Lyme raises anti-neuronal antibodies as well as cam K? Or is it only cam k if uncomplicated Lyme ?

 

[lss]

I asked Dr. C a question very similar and this was her reply:

 

Dr. Cunningham,

 

Seems a whole new discussion is circulating in the Pandas (among parents) world and it appears that almost all of the Pandas children are turning up positive for Lyme as well.

 

Could it be that the antibodies in Pandas may cross react with Lyme testing?

 

Dear Linda

 

There could be crossreactivity with the organism

causing Lyme disease but this may mean that other

infections such as Borrelia burgdorferi can induce these

antibodies also. Certain viral infections may also be culprit

too. If he was neg on western blot, then he is probably negative

for Lyme. If there is crossreactivity, then we will not be sure if it

is strep or Bb or a virus. It can be complicated but the thing that is

certain is the anti=neuronal antibodies and their correlation with disease.

 

I am testing some Lyme sera and will have more definitive results this fall.

The Lyme sera I have tested are in the PANDAS range. I will need to do more.

 

 

 

Hope this helps.

 

Linda

[norcalmom]

It looks like yes, it can cause it, but it also looks like just the infection itself can cause symptoms at lease as related to cardis and arthritis. I'm not 100% sure. Here is a mouse study she did in 2005.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC548028/

 

the way I read it - the infection causes inflamation and tissue response in both an autoimmune prone mice, and non-autoimmune prone mice, but the one with the autoimmunity problems will get it worse.

 

"Overall, our results show that an autoimmunity-prone NZB mouse can develop a greater degree of clinicopathologic features than a non-autoimmunity-prone mouse. Furthermore, there is a greater antibody response to the inciting infectious pathogen, B. burgdorferi, which is cross-reactive with host tissue."

 

Her lyme studies seem to focus more on arthritis and cardis. They measure the joints after infection, and then biopsy the heart and count the cells. No mention of the type of neuro-phychiatric symptoms our kids have.