Question about Lyme disease

[Guest pandas16]

Could someone just affirm whether or not I'm correct or not- with PANDAS, you have this persistent L-form of strep which results in molecular mimicry and then triggers auto-antibodies/inflammation etc. In Lyme there's also an L form as well or sprichote form that also leads to inflammation etc? So is it the sprichote that causes the neuro pych sypmtoms in chronic neurological Lyme or the autoimmune response/inflammation that the sprichote causes? Also is it possible that tindamax/flagyl are killing the L form of strep?

[MichaelTampa]

I'm not sure much is known about the pandas side of your question, in any event, I don't know anything about that. I But that is an interesting idea to explain why the ongoing abx would work, in essence, by keeping the strep in L form.

 

On the lyme side, there is a cyst/inactive form, which I believe is also called the L form. This contrasts with the active spirochete form. Flagyl/tindamax do fight the cyst form. On the neuropsych symptoms for lyme, there is probably much more speculation than real knowledge. I have heard the neuropsych attributed bartonella, but also to the lyme (borrelia). I haven't hear people speculate in terms of active vs. cyst form. It does seem many do believe the neuropsych symptoms (and other symptoms, such as pain and so on) really are from inflamation rather than the bugs themselves.

 

But now very recent evidence confirms that CCSVI, blockages in veins in neck returning blood from brain, plays a huge role in neurological symptoms, and I'd love if people would be clear if they meant neuro symptoms other than the neuropsych symptoms, or if they meant all neuro symptoms, even the neuropsych symptoms. It was discovered in 2009 that neuro symptoms of MS are caused by this CCSVI blockage, and as some in the lyme world know MS is caused by lyme, lymies with neuro symptoms are being tested, finding they all have this CCSVI blockage as well, and some have had amazing elimination of neuro symptoms by clearing this blockage with angioplasty (although the symptoms return in some cases, as the blockage can returns). They view low-oxygen blood trapped in brain for the neuro symptoms. But still, this doesn't rule out inflamation as the ultimate causes, as perhaps this low-oxygen blood results in inflamation...

 

The problem with being sure with so much of this stuff, is, the tests for strep and lyme and bartonella are so bad, people go by symptoms, and then use antibiotics that are more broad-spectrum than specific against any one bug. So, we just have this picture of people having these symptoms, taking these things, get this result. People have built a lot of "understanding/stories" around this, assuming it is a particular bug being acted on by a particular antibiotic, and then when symptoms disappear, they think they have learned what caused what, but this whole understanding is built on something, well, sturdier than a house of cards, but not with a real solid foundation either.

[KaraM]

I asked a similar question of our LLMD regarding Bartonella.

 

I was confused whether the same thing was with Bartonella as was happening with PANDAS - where the antibodies attacking the brain result in the inflammation of the basal ganglia and then the neuropsych symptoms

 

I asked if that what was happening of if the infection was actually in the brain. She said she thought it was the infection in the brain...so not the same as PANDAS.

 

I don't know if she's right or wrong...but those were her thoughts..

[rowingmom]

My understanding is that there are 3 forms of lyme. The spirochete, the cyst form, and the acellular L-form. Lyme infection can cause the development of autoimmune reactions. Whether lyme or bartonella are causing DD9's motor tics (so they would be classifies as PITANDS), I don't know but her tics have been improving on biaxin/banderol/samento. She will probably start herxing when we begin rifampin and the tics and bart symptoms will increase. I have heard nothing from my LLMD that this might be an actual brain infection. I will have to ask. Flagyl is used to attack the cyst form, don't know how it effects L-forms.

Edited July 7, 2011 by rowingmom

[LNN]

My understanding is that there are 3 forms of lyme. The spirochete, the cyst form, and the acellular L-form. Lyme infection can cause the development of autoimmune reactions. Whether lyme or bartonella are causing DD9's motor tics (so they would be classifies as PITANDS), I don't know but her tics have been improving on biaxin/banderol/samento. She will probably start herxing when we begin rifampin and the tics and bart symptoms will increase. I have heard nothing from my LLMD that this might be an actual brain infection. I will have to ask. Flagyl is used to attack the cyst form, don't know how it effects L-forms.

Yes, three forms of lyme is my understanding as well. Extracellular abx tend to work on spirochetes, tindamax and flagyl work on cyst forms and intracellular abx like zith, bactrim work on l-form. It's one reason behind using combos of abx for treatment. if you only use extracellular abx, the lyme goes into cyst until you stop that abx then comes out of hiding. The combos are meant to attack the various forms simultaneously. But there are also biofilms, which are extremely hard to fight even with absurd amounts of abx.

 

I have read in various places about evidence of spirochetes being in brain tissue as well as spinal fluid (the stories in Cure Unknown of the Alzheimers and ALS patients for example). So nothing says it can't be an actual infection of brain tissue. But it could also be inflammation triggered by the infection or triggered by autoimmunity. Heck, they can't even develop reliable tests for the disease, let alone tests to tell what else is going on.

 

Pandas16 - I'm not familiar with the thought that Pandas is a result of a chronic l-form of strep. Rather, I understood it as an autoimmune response to GABHS that can continue for a time after the actual strep is eradicated, due to an unregulated or under-regulated cytokine response. If L-form bacteria were suspected as a culprit, my understanding is that augmentin and other extracellular abx wouldn't be effective, since they work on the outer surface of the bacteria, which doesn't exist in an L-form bacteria. Do you have a different understanding?

[sf_mom]

From the rumor mill: There was discussion of L form Strep at last summer's PANDAS get together... Unfortunately, everyone acknowledged its existence but nobody seemed to know how treat. I remember this because the thought was paralyzing to me at the time.

 

Here is a great video on how Lyme Disease leads to inflammation and also a general overview on treatment. Worth the 7 minutes to watch and simple enough for most to understand a complicated disease.

 

[LNN]

SOMETHING was pushing the auto-antibody production even though i actively didn't feel sick. Right? What else could it be if it's not some sort of intracellular microbe. I know that cytokines weaken the blood brain barrier. That makes a lot of sense but it shouldn't matter if there aren't autoantibodies? Is chronic neurological lyme just an autoimmune disease too?

 

No, I don't think chronic lyme is just an autoimmune disease. I think (personal opinion) that it's an active infection that's above a certain threshold. I suspect lots of people walk around with low levels of lyme and co-exist, without major symptoms, or clear it entirely. But when the lyme reaches a certain volume, and the body can't keep it in check, it becomes something you need to beat back down. Maybe never eradicate, but get back a bearable level. I think the video Wendy posted helps explain how it can also become autoimmune, but my personal thought is that if you can beat the stuff down to a minimal level, the autoimmunity piece becomes negligible or non-existent. I don't think neuro lyme is simply autoimmunity. But I do think it's a very strong reaction to inflammation that's messing up the brain chemistry. Maybe that inflammation is due to an autoimmune reaction within the basal ganglia or maybe it's due to an active infection within the brain or CNS. I'm not sure there's any way of knowing without putting my DS's brain under a microscope. So for now, I'll do what I can to kill bacteria, support his own immune system, help his body clear toxins and reduce inflammation. My thinking may change as time goes on, but that's where I'm at at this point in the journey.

 

There's one other point I want to raise, and I ask this with no agenda. I'm not suggesting you have lyme (tho I do hope if your symptoms continue, you consider ruling it out). But in your comments about an on-going intercellular infection, you make an assumption that auto-antibodies must be behind your episodes. At one time, I would have agreed with your thinking. But having seen my own son's journey, maybe you want to re-assess that assumption. Could the first part of your statement be correct "there must be some sort of microbe" but the second part be wrong that "it's pushing auto-antibody production." What if auto-antibodies aren't the problem. What if an active infection from something other than strep is at play in your body? Again, I'm not trying to diagnose you or argue or push an agenda. It's just meant as a question to ask yourself because I "wasted" time trying to fight a battle only on one front (Pandas/strep) only to find out there was a second front and a second enemy (lyme et al) that had made gains while I was fighting the first war. You might be entirely correct and I know you've seen the top names in the Pandas field. We've worked with many of them at various times and they were all helpful in their own way. But due to their specialization, none of them looked beyond strep. My own assumptions were one of the roadblocks my son had to overcome. So I just ask because when you let go of what you think you know, the ballgame sometimes changes. Just food for thought.

[LNN]

I think for at least some of us here, there is more than lyme at play. Thus, the threads about KPU and mold and other insults. For me, it's a matter of lightening the load until my son's own body can support itself. It means killing stuff, clearing stuff with detox and making his own systems stronger. It may never mean having a squeaky clean system. Just one that can function well.

 

I don't believe the problem is solely inter-cellular. I think it's way too complex for just one thing to be at play. And highly individual. I think the "proof is in the pudding" and when a family finds something that works, then they need to pursue it and share the ideas with others. But it doesn't mean it's "the" answer for everyone. Not everyone who comes here will find their "aha" moment. Lyme treatment can be unpleasant. No question. So is training for a marathon, studying for a state board exams, rehabilitating from a serious injury...what makes lyme treatment right for some is that little by little, you get to a better place. But everyone needs to find their own lock and key. And for some, it's more than one lock. It's more like those Russian dolls that nest inside one another. We crack open one doll only to find another. But I do see big changes from where we were three years ago. So we keep cracking...

[LNN]

How is your child though? If you don't mind me asking. I don't really know your whole story. Can he/she go to schools? Does he have tics/OCD? Like how far has Lyme treatment brought him?

Three years ago, he was debilitated by anxiety and no therapist could help him. His daycare provider once used the word "sociopath". He had no impulse control, and at his worst, we called him "Linda Blair". He curled up under the coffee table in fear and rage. He had severe motor and vocal tics, moderate OCD that interfered with school performance (tho he could attend school). He could barely hold a pencil and his teacher suspected asperger's. He was 6 months below grade level.

 

Today, he is at grade level, he has no anxiety, is OCD-free 99.5% of the time (and is sub-clinical for the other 0.5% - no one sees it but him and me and on a YBOCS scale would be below 10 even on a bad day when he was once high 20s), went 18 months without tics (which returned when we started tindamax but resolved when we stopped - probably herx related). He uses CBT very effectively for anger management. His biggest remaining issue is brain fog, which is why we're looking into pyroleuria/KPU, since he developed tardive dyskenesia when he took zicam for a cold - so very weird reaction to zinc). When we first started bartonella treatment last fall, his reading jumped 7 levels while his peers jumped 4 levels (thus, he caught up and no longer requires tutoring). His reading fluency jumped from 67 wpm to 140+ wpm (but declined to 104 wpm when he had his bad herx/return of tics). He still has things to work on. We haven't reached the finish line. Brain fog continues to rear its ugly head far too often. But I'll take "mom, I don't feel right" over "I can't come out from under the coffee table" any day.

 

I don't just credit lyme treatment. We've done abx and prednisone for Pandas, pheresis, IVIG, bartonella treatment, lyme treatment, detox, CBT and ERP therapy, tutoring...and there's also the benefit of maturity. He was 5 when this started and is almost 9. No single thing was the magic bullet. It's a cumulative thing and we continue to work toward a goal of being abx free and healthy. There's more pain ahead, I'm absolutely certain. I'll be here next month with a knot in my stomach, questioning and needing support. I don't claim to have answers for anyone else. I just know most of what we've tried has helped for our situation (my one exception is IVIG, which was a very bad experience and puts me in the minority).

 

My 6yo daughter also has health challenges, more with intrusive thoughts and gastro. Her path is less clear but also less severe. So I talk about it less often. We're still trying to figure her out.

[SSS]

Just wanted to pop in, as I read the board over here, and say thank you LLM for sharing your story, and for your posts- I think you are valuable here on these forums.

Part of the journey for my daughter and her immune system is mercury- I find it interesting that Lyme Dr.'s test for heavy metals as part of the protocol...yet it is not discussed as much?

I have done a hair test, dmsa urine toxic metal test, and 2 porphyrin tests from a lab in France, and all indicate she is holding on to mercury (excessive amounts.) She has had the exposure to back up these findings.

Part of our path to wellness is getting this level down, which I am planning to attempt over the next year with low, frequent weekend chelation.

Also had our blood draw yesterday for a look into lyme/bartonella.

I personally think the heavy metals are tied into all this.

Anway, thank you all for sharing your intelligence and experiences, it truly helps the rest of us.

[MichaelTampa]

Yes, for sure heavy metals are part of it, and yes, it seems we talk very little about them. I think many llmd's don't really deal with it, and probably do not understand it is an important part of the picture--similar to parasites. I imagine this is part of why treatment takes so long for some people, and some never get healed.