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» LymeNet Flash » Questions and Discussion » Medical Questions » MS Patient Now on ABX; Feeling Horrible

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Author Topic: MS Patient Now on ABX; Feeling Horrible
marcstck
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Hello folks, this is my first post. Hoping to get some info here on the rigors of antibiotic treatment.

Four years ago, I was diagnosed with Primary Progressive Multiple Sclerosis, a rare form of the disease marked by a steady progression of symptoms rather than relapses followed by recovery. My MRIs have been unchanged in four years, and show one small lesion in my brain, and one large lesion in the upper cervical spine. My spinal taps have always proved negative for MS. Four years ago, my symptoms first presented as a slight limp in my right leg. Now, after 48 months of unrelenting progression, my right arm and leg are basically useless, and my left side is now starting to weaken as well. I fear I will be a quadriplegic within 12 months if this progression can't be stopped.

None of the standard MS treatments have worked for me. I've tried interferon, spinal injections of methotrexate, Tysabri, and plasmapheresis. None have done anything to slow or halt the progression of my disease. The one thing that did provide symptom relief was 10 days of IV steroids, which also left me with avascular necrosis, a painful condition of the joints. Some doctors have used this as evidence that I do not suffer from Lyme disease, as conventional wisdom holds that steroids would only make the Lyme worse.

As I have never been comfortable with my diagnosis of primary progressive multiple sclerosis, I have sought out other opinions through the years. This past March I saw a noted LLMD (Dr. P. in Connecticut) who thought I might be suffering from Lyme and ordered a battery of tests. My Igenix Lyme tests came back negative (only two positive bands), but the doctor's interpretation of them is that they may indicate a chronic Lyme infection. My CD 57 tests also came back normal, but at the very very low end of normal, which the LLMD also interprets as a sign of possible chronic Lyme infection.

My MS neurologist is not a believer that I have Lyme. However, we've pretty much run out of options as far as standard MS treatments go, and my neurologist has become convinced that immunosuppressive therapies do not work in my case. He's therefore agreed to prescribe antibiotics for me.

On the advice of the Lyme doctor, I started on minocycline (100 mg 2x per day) last week. Within two days, I felt like I could die. Nauseous, dizzy, spaced out, night sweats, and my MS symptoms worse than ever. I'd heard about the Herxheimer reaction, and didn't know if I was experiencing a Herx or side effects from the medication. I spoke to the LLMD, and he decided to switch me to doxycycline (100 mg 2x per day). I started the doxy last Wednesday, and felt slightly better than when I was on the minocycline. By Saturday, though, I was again feeling miserable. I barely had the strength to get out of bed. I was completely devoid of energy, and my MS weakness left me almost immobile. I decided to skip my nighttime dose of doxy, and woke up feeling like a truck had hit me. I took my morning dose, and am trying to get through the day.

Does this sound like a Herxheimer reaction? Or could this be the result of side effects, or possibly an allergy, related to the meds? This reaction has been most upsetting, but I am desperate to get some relief as I feel like the clock is ticking in regards to the progression of my disease. The prospects of becoming a bedridden lump of flesh seem very real to me, and I must admit that at this point I am feeling desperate...

Thanks in advance for any help you folks can give...

Posts: 6 | From new york city | Registered: Aug 2007  |  IP: Logged | Report this post to a Moderator
chamade
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This does not sound like any kind of allergy, but a typical herxheimer reaction. I hope you're on the right path.

--------------------
Why me? Well, why not me???

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pineapple
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Welcome to Lymenet. First, I am sorry you have seen so much progression and your treatments have failed thus far. Very frustrating for sure!!

I am confused why they would diagnose MS with so few lesions. I have multiple lesions in the brain from Lyme but have never officially been diagnosed with MS.

What you described sounds exactly like a herxheimer.

There is considerable evidence suggesting a strong link between MS and Lyme disease. I am saddened that they waited so long with you to try antibiotics.

Here is where you can get started with your reading:

http://flash.lymenet.org/scripts/ultimatebb.cgi?ubb=get_topic;f=1;t=041500

Someone will come along and answer your question better than I. I am wearing down at the moment and need a nappy.

Please stick around and read, read, read!

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chamade
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BTW, it seems to me that you should be on IV antibiotics. Did your LLMD ever mention this, is he just taking it easy for now?

--------------------
Why me? Well, why not me???

Posts: 411 | From San Francisco, CA | Registered: Mar 2007  |  IP: Logged | Report this post to a Moderator
valymemom
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I know the llmd you are seeing has worked with folks who have been diagnosed with MS or have MS kind of symptoms. I would trust his judgement.

If you read/do a search on detoxing, you will see that besides the abx, you need to add supplements for getting rid of the created toxins......chorella and chitosan are two that come to mind for a search.

MS is a more physician directed illness - tickborne illness requires so much research on our part. All our llmds strive to understand these pathogens but I do not believe any one of them has all the answers. Each of us is so individual.

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Vermont_Lymie
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Sounds like a herx reaction to me. I agree with the other poster who mentioned IV abx.

Important to detox as you can while herxing on antibiotics. If you do a search here under "detox" you will probably get 100 posts to read with a range of information, from the truly useful to interesting. Although it may be difficult while you are feeling so awrful, take the time if you can to read alot.

Take care and sorry to hear that you have been so ill.

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Jellybelly
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Hi, my mom was also been given a diagnosis of MS. I took her to my LLMD as she lived in the same area I contracted Lyme and actually remembers a bull's eye rash many moons ago.She has numerous lesions in her brain and one or two on her spinal cord. She also has some serious neropathy.

Her first WB, came back totally negative for anything. But, LLMD really believed that she had Lyme and started her on ABX anyways. Had her retested after one month for the Lyme and this time she came back CDC positive. This happens often with Lyme testing. ABX seem to help some how in getting the immune sytem to make it's own antibodies.

She was put on an ABX as I stated and herxed pretty much right off the bat. It put her to bed, where she had not been for awhile because Avonex did work for her. She kept it up for about 3 months, and felt really bad the whole time.

She finally had to stop, but after the herx quieted back down she found she had some major reversal of some symptoms. One that stands out is that she started gaining feeling back in her feet in particular which were absolutely not able to sense touch, even when something sharp was stuck in her foot.

Also there was a marked reduction in swelling around her joints. Can't say her joints look particularly pretty now as the damage that had been done already is now clearly visible. But they felt better.

She has recently gone back on the Avonex as opposed to taking more ABX. I guess her reasons are, that she is 69, and may not have that many years left no matter what. She doesn't want to spend what time she does have in bed due to herxing. I do have to agree in this case.

BUT, if you have no other option as it sounds you may be there, ABX were amazing for her. She even went dancing before she started the Avonex back up, and she hadn't done that in I don't know how long due to pain. Walking was becoming more and more difficult all the time.

I am sorry you are so sick, but I do whole heartedly believe you are heading in the right direction. [Smile]

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TerryK
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I'm sorry you are so sick.

Were you tested for co-infections too? The tests are not all that reliable but if something did show up, it would be meaningful towards a lyme diagnosis not to mention would point to further treatments that will help you recover your health. That said, you can have one of the co-infections without having lyme. Many are treated via a clinical diagnosis of co-infections and lyme too for that matter.

I've been on abx for 15 months and the herxing has been brutal the whole time. Apparently the toxins that are produced by the dieing bugs are causing the herx symptoms. Metals being released from dieing bugs are causing some symptoms too.

About 25% of the population cannot detox very well from these toxins. There are genetic tests that one can have to verify if this is a problem for you. My sister was tested and found to have the problem and given my response to abx, we are sure that I also have a problem with detox.

My LLMD has me on cholestyramine for the biotoxins. I'm also on drainage remedies for the intracellular debri and metal binding and removal supplements. It helps to have the use of both an ND and an LLMD in order to deal with the affects of treatment.

One can also have a reaction to the medication so it pays to keep in close touch with your LLMD.

Learn as much as you can about this beast so that you can learn what you need to do to give it a good try at treatment. I hope it is the answer for you.

Terry

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marcstck
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Thanks for the responses, folks. They've been most helpful, and encouraging. I'm quite confused over the proper course to take. I've been seeing a renowned MS neurologist for the last three years, and I'm reticent to do anything to jeopardize my relationship with him. But, he's not a believer in either the Lyme or chlamydia pneumonia theories related to multiple sclerosis. As I said, he's agreed to antibiotics simply because we've run out of other options. He does not know that I've seen a LLMD.

I prefer not telling my neurologist about the LLMD, because he's working on some very progressive treatments for demyelinating diseases, involving neuroprotection and neuroregeneration, and I'd like a crack at them when they become available. However, it does seem like this can get a bit tricky. My LLMD has indicated that he'd like to see me on intravenous antibiotics. I'm pretty sure my neurologist won't come to the same conclusion. Seems like I'm going to be reaching a crossroads soon, and I also feel like I'm carrying on an extramarital affair. It's hard enough being sick, without having to deal with all this other crap...

I have been tested for co-infections, and those tests all came back negative. I did test positive for chlamydia pneumonia, but my understanding is that the vast majority of American adults are positive for that bug. As I said, I've never been comfortable with my diagnosis of PPMS, as my presentation has been atypical even for this strange disease. I'm grasping for answers, and fervently hoping that antibiotics will eventually give me some relief. Looks like it's going to be a hard road to follow, though...

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oxygenbabe
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The question is, with this much damage to your system already, even if it was/is triggered by a bacterial infection, does a "herx" that puts you in bed even worse than ever from the toxins, mean that your system will be crashed? I remember someone with ALS from lyme, who did IV rocephin, and tho cognitive function improved, the toxic load to his body was so bad he simply got worse on it.

Also consider fungal toxins.

I don't really know why I'm saying this but what about the Schardt protocol? A course of diflucan and then a course of penicillin. Dr. P in Connecticut *has* used it.

Just a feeling I can't explain, that you might want to try antifungals.

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Lymetoo
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Welcome! I'm sorry you're going through this. I can imagine you feel like a guinea pig by now!!

One thing to consider about the test result is that you have been given a LOT of immune suppressing drugs over the years. That would definitely make a Western Blot for Lyme show less than positive.

Could you look for that test and tell us WHICH BANDS showed positive. That is VERY important.

I agree that what you described is a classic herxheimer, in my humble opinion.

200mg of minocycline is a high dose to begin with. 200 mg of doxy is low.

You may want to go back to mino later at a lower dose to start out with and then build up to 200mg. [my non-medical opinion]

By the way, you are in good hands with Dr P!

Here is some info for your reading pleasure!!

Dr. Bransfield's Reason's for Seronegativity the reasons why you can test negative and still have Lyme disease.

1. Recent infection before immune response
2. Antibodies are in immune complexes
3. Spirochete encapsulated by host tissue (i.e.: lymphocytic cell walls)
4. Spirochete is deep in host tissue (i.e.: fibroblasts, neurons, etc.)
5. Blebs in body fluid, no whole organisms needed for PCR
6. No spirochetes in body fluid on day of test
7. Genetic heterogeneity (300 strains, 100 in U.S.)
8. Antigenic variability
9. Surface antigens change with temperature
10. Utilization of host protease instead of microbial protease
11. Spirochete in dormancy phase (L-form) with no cell walls
12. Recent antibiotic treatment
13. Recent anti-inflammatory treatment
14. Concomitant infection with babesia may cause immunosuppression
15. Other causes of immunosuppression

16. Lab with poor technical capability for Lyme disease
17. Lab tests not standardized for late stage disease
18. Lab tests labeled "for investigational use only"
19. CDC criteria is epidemiological not a diagnostic criteria
20. Lack of standardized control
21. Most controls use only a few strains as reference point
22. Few organisms are sometimes present
23. Encapsulated by glycoprotein "S-layer" which impairs immune recognition
24. "S"- layer binds to IgM
25. Immune deficiency
26. Possible down regulation of immune system by cytokines
27. Revised W.B. criteria fails to include most significant antigens

You may also have babesia, which would require the use of different meds than for Lyme. NIght sweats are one of the many symptoms. You do NOT have to have all of these symptoms for it to be babesia. Many of us are 'blessed' with more than one illness from the tick.

The following signs/symptoms may be present in those infected with Babesiosis:
Fatigue*
Arthralgias*
Myalgia*
Drenching sweats*
Headaches*
Emotional lability*
Depression*
Dark urine*
Splenomegaly*
Dizziness*
Nausea and vomiting*
Cough*
Dyspnea*
Fever*
Chills*
Hepatosplenomegaly*
Jaundice*
Malaise*
Shortness of breath*
Bleeding tendencies,
bruising*
Thrombocytopenia*
Hemoglobinuria*
Hyperesthesia*
Pulmonary edema*
Encephalopathy*
Low to normal range leukocyte counts*
Possible elevated levels of dehydrogenase, bilirubin,
transaminase*
Anorexia*
Approximately 25%- 66% of Babesia patients are known to be co-infected with Lyme disease. These symptoms may continue for long periods of time, decrease, then return. A low Babesiosis titer (IgG) often indicates a chronic infection.
An acute or current infection may show a higher reading on the IgM test initially. There are over 100 species of Babesia in the United States but only ONE or TWO species are currently checked by commercial labs.

Lyme Disease Symptoms List
1. Unexplained fevers, sweats, chills, or flushing
2. Unexplained weight change--loss or gain
3. Fatigue, tiredness, poor stamina
4. Unexplained hair loss
5. Swollen glands: list areas____
6. Sore throat
7. Testicular pain/pelvic pain
8. Unexplained menstrual irregularity
9. Unexplained milk production: breast pain
10.Irritable bladder or bladder dysfunction
11.Sexual dysfunction or loss of libido
12.Upset stomach
13.Change in bowel function-constipation, diarrhea
14.Chest pain or rib soreness
15.Shortness of breath, cough
16.Heart palpitations, pulse skips, heart block
17.Any history of a heart murmur or valve prolapse?
18.Joint pain or swelling: list joints_____________
19.Stiffness of the joints, neck, or back
20.Muscle pain or cramps
21.Twitching of the face or other muscles
22.Headache
23.Neck creeks and cracks, neck stiffness, neck pain
24.Tingling, numbness, burning or stabbing sensations, shooting pains
25.Facial paralysis (Bell's Palsy)
26.Eyes/Vision: double, blurry, increased floaters, light sensitivity
27.Ears/Hearing: buzzing, ringing, ear pain, sound sensitivity
28.lncreased motion sickness, vertigo, poor balance
29.Lightheadedness, wooziness
30.Tremor
31.Confusion, difficulty in thinking
32.Diffculty with concentration, reading
33.Forgetfuiness, poor short term memory
34.Disorientation: getting lost, going to wrong places
35.Difficulty with speech or writing
36.Mood swings, irritability, depression
37.Disturbed sleep-too much, too little, early awakening
38.Exaggerated symptoms or worse hangover from alcohol

Wild Condor's Links and information:
http://www.wildcondor.com/lymelinks.html

 -

--------------------
--Lymetutu--
Opinions, not medical advice!

Posts: 95327 | From Texas | Registered: Feb 2001  |  IP: Logged | Report this post to a Moderator
kitkat32
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Hello there and welcome.

I was also diagnosed with MS. I had always had negative MRI's and negative spinal taps. My neuro said that there was nothing else to explain my symptoms.

I was treated for several years with prednisone and solu medrol.

My symptoms became so crazy and non MS like that my well known MS neurologist told me flat out he didn't think it was MS anymore. He agreed to have my testing sent to Igenex. I have many IND bands..below weak positive but does show something.

I was scared to change from my MS diagnosis to my possible lyme. I didn't want to jeopordize the relationship I had with my neuro.

I finally just made an appt. with him and told him that I was going to see a LLMD. I told him that it might be against his advice but it was a treatment that I needed to try.

I told him that I wanted to stay in a good patient/doctor relationship with him and if things did not lead in the direction of Lyme we could pick up were we left off at trying to find out what is wrong.

Having kept my relationship with him gave me piece of mind. You have to remember they don't own your body and it is up to you what health road you choose.

I am glad that I made this decision. Alot of my so called MS sx have disappeared since starting my lyme treatment. I am still not where I want to be but I am better than I was.

I no longer have weakness in my arms and legs..except during a med change with a herx.

It won't hurt you to take the abx road. Anti-biotics..in my non medical opinion..isn't as bad for you as everything we have taken for MS.

I hope this helped.

Good luck to you...kit

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CaliforniaLyme
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WELCOME*)!*)!*!)!
!*)*!)!))!!

I know many people who are Lyme/MS and have done great with antibiotic therapy!!!!!!!!!!

In my experience what you are describing is a Herx and if you back off you won't get the benefits- that is the way it worked for me anyway- I used to repeat my herx mantra,
"The only way out is through!"*)!*)!*

I hope you see gains quickly but it takes time for many of us!!!

Glad you are here(_!!!!!!!!!

--------------------
There is no wealth but life.
-John Ruskin

All truth goes through 3 stages: first it is ridiculed: then it is violently opposed: finally it is accepted as self evident. - Schopenhauer

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oxygenbabe
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Also, if antibiotic therapy or antifungal doesn't work, Patricia Kane has worked with people who are losing neurological function. I recently read of one case of bodywide myositis, in which you basically lose muscle function, in which she used her IV phosopholipid/glutathione protocol, leucovorin and other methylation supplements, and sent the person to an immunologist for IVIG----and after intensive treatment that patient is well on the road to recovery, still getting maintenance treatments. This approach restores immunity and the cell membrane.
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lymednva
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Last fall many of us met in Valhalla, NY for a protest against IDSA (Infectious Diseases Society of America).

One of the women who spoke had been dx'd with MS and had been basically bed-ridden, as I recall. She, at that time, was using a scooter and gave a powerful speech.

I recall she said her husband had not been able to understand her speech prior to her Lyme treatment. She was easily understood that late November day.

I hope someone else who was there will add in some more details about her.

I'm not a medical professional, but it sounds like in your heart you know that you don't have MS. I would go ahead and get that IV treatment, in hopes of turning things around before it is too late.

Good luck to you!

--------------------
Lymednva

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Lymied
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Hi marcstck,

I had a lot of neurological symptoms when I became acutely ill.

I started on 100 mg of doxy just two times a day...I had such bad reactions that I literally thought I was dying. I had heart palpitations, problems swallowing, such bad pain I had to crawl up stairs, spontaneous swelling of joints in my hands that you could literally see swell with in a short period of time, parathesis where it felt like I had a tournaquet around my arm, as well as such disconnected feelings that I could not drive temporarily.

Turns out it was a huge herxheimer and doxy was a medication I took with other antibiotics to get well. The reactions became less and less each time I took it.

Hang in there and feel lucky that you most likely are on the right treatment track and there is hope that others that have been misdiagnosed have not had.

I remember laying in bed talking to a friend of mine in NH when I was so ill and having wild herxheimers...she told me that some of my symptoms sounded like a friend of hers in his thirties who has MS. I remember being petrified. I think of him all the time now that I am getting back to a somewhat normal life again.

I asked that she forward info. to him about lyme but I don't think she ever did.

Anyway, take care and hang in there. I would continue the treatment if I were you.

--------------------
Pride is concerned with who is right. Humility is concerned with what is right. - Ezre Taft Benson

Posts: 655 | From NC, Exit 88 on the Deer SuperHighway | Registered: Dec 2004  |  IP: Logged | Report this post to a Moderator
sixgoofykids
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I'm sorry you're feeling so ill. I second Lymetoo's suggestion of posting which bands are positive.

I would give the LLMD a chance. You've given the MS doctor years and have seen degeneration. The Herxheimer Reaction can be considered to be confirmation that it indeed is Lyme Disease that you are dealing with. If you didn't have Lyme, you wouldn't have herxed.

I'd simply not make another appt. with the MS doctor ... see the LLMD for a while ... if you want to go back to the MS doctor later, just tell him you tried some other stuff and now you're back.

--------------------
sixgoofykids.blogspot.com

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savebabe
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Most of my docs originally thought I had MS due to optical neuritis.

It wasn't until my friend(a nursing student) suggested that I get tested for lyme by a llmd. So off I went to East Hampton.

Now with a proper diagnoses of lyme,babs and bart, along with aggressive treatment, many of my MS symptoms have disappeared.

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AliG
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Welcome!

Like Tutu, I thought Babesia when I heard night sweats. After taking down my Babesia, my LLMD started out slow with 200mg Doxy then worked up to 300mg. Which gave me manageable Herxs.

I'm sure with the treatments for MS you're probably in a lot deeper than I was off the bat. I believe it was because of my neurological symptoms that my LLMD has chosen to go slowly.

Too much die off too quickly can put a heavy burden on the immune system to clean up. I believe someone earlier mentioned that they were familiar with your LLMD and that you are in good hands.

Sometimes it takes a little time initially to get a good balance with the antibiotics & the Herxs to keep it manageable.

Make sure you are drinking plenty of water to help flush out the die-off. Take some good probiotics (not within 2-3 hours of ABX) and take a good multi-vitamin along with some extra antioxidants(also not w/in 2-3 hrs).

Afternoon naps are also important for fighting the battle. I have also found that when joints really hurt, I try to move them a lot and this seems to flush out whatever's going on in there.

I would say that what you describe sounds really encouraging that you are on the right track.
The thing I tell myself when things seem really tough is "this too shall pass" [Smile] . For every awful herx, you're that much closer to better. [Big Grin]

I really hope you see improvement soon. That's when YOU'LL really know you're doing the right thing. [Big Grin]

Best Wishes,
[hi]
Ali

PS - The links you've been given are truly worth reading.

--------------------
Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner.

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Boomerang
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Welcome! Glad you found this group. Hubby was tested for possible MS, but everything came back negative for it. The Igenex tests showed positive bands, so he has been on ABX for Lyme.

Sure sounds like you had quite a reaction to ABX, which indicates a bacterial infection. Doesn't sound like an allergic reaction to me, and I've seen hubby have some allergic reactions.

You probably need to start out slow on oral ABX and see how you respond, then do IV at some later point.

Also probiotics and detox.

Take care.

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marcstck
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Thanks again, folks, for all the great info. I feel like I may finally be on the right track, despite my current crummy condition. My neuro is supposed to get back to me this week regarding an antibiotic regime that he's researching; I suspect he will recommend something the lines of the Vanderbilt protocol for chlamydia pneumonia infection. As I said, he doesn't know that I've consulted with a LLMD, and is convinced that I do not have Lyme disease due to my CDC negative blood test results. I'm hoping that the ABX that he prescribes will match up with the ones that the LLMD prescribes, and that there won't be any conflict. If the recommendations turn out to be too disparate, I may be forced to tell the neuro about the LLMD...

I'll try to post my Igenix results tomorrow. Hopefully, I'll have enough energy to get out of bed and dig them up. It will be interesting to see what you guys make of them...

I certainly hope that what I'm experiencing is in fact a Herx. Is there any way to know for sure?

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Myco
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This is a typical herx and a GOOD SIGN : )

Please see CPNHELP.ORG for support from other MS patients on antibiotics. I think their protocol is THE BEST and most of them are well on their way to remission, if not already. Their's is DOXY, then adding in Zithromax, and eventually Flagyl. This would take care of Lyme or CPN. Both implicated in MS.

Best,

Chris

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tory2457
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Hi marcstck and Welcome:

I too have MS for 20+ years; flunked my IgeneX test, but had positive bands!

My doc is Dr.P too, and I am getting better. This after being on a DMD prior to seeing a lyme doctor. I have lesions on my brain and spinal cord; have numbness, tingles, TN, to name a few..

I also tested negative for Babesia and Bartonella, but testing for co-infections just like testing for lyme are not very reliable..
My body tells me that I in fact have Babesia, Bartonella, and probably "other" co-infections..that typically go along with Lyme..

imo, I would remain a patient of Dr P, he's smart knowledgeable and I am confident he will make you better too!

From what I've read and talking to Dr P, his belief is to get the bacterial load down as quickly as possible; meaning go as fast as you can tolerate!

Personally, I feel this way about Dr P [bow]
on another note: My sister-in-law who has Sjogren's, RA, IBS, Fibro finally after years of suffering went to a lyme doc; tested negative by IgeneX-with positive bands, but tested CDC positive for Babesia! and the CDC called her.

My understanding is: you don't have Babesia without having Lyme Disease..oh yes, a year ago after I was diagnosed she went to her Neurologist, he tested her at Quest for Lyme, it came back negative (of course) and he vehemently told her to "get off the internet" with the quacks that push Lyme Disease. SHAME ON HIM! She too is getting better!

Feel free to pm me anytime; we can compare notes!
[Wink]

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tory2457
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Marcstck:

oops, forgot to mention. I too had 2 of the finest Neurologist in the Philadelphia area. Both are in research and speak regularly across the US.

I also found it difficult to come to terms that these fine doctors talked to me about avoiding a wheelchair as I grow old (the reason to begin DMD's) yet missed the mark of an infectious cause! It did and kindof still does mess with my head! They are supposed to be one of the very best! hmmm

Thanks Dr P!

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Visual Afterimage Man
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I'm sorry you feel so horrible!! There is so much information on this thread that I had to go back and re-read what you said your antibiotic doses were. (lyme brain causes me to forget a lot of things)

What caught my attention is that you are on a fairly low dose. If you found yourself feeling that horrible on a low dose of mino or doxy, then it stands to reason that it is most likely not a reaction to the drug, but a reaction to the massive die off of bugs that were in your system.

Also think about a typical allergic reaction. Hives, swelling etc. A flair in your current symptoms is indicitive of a herx. Don't be surprised if a herx brings out NEW syptoms that you never noticed before.

Its such a mind game.. because there is no diffinitive answer as to what you are going through. I just encourage you to listen to your LLMD's advice, and really think about your situation. Make a log and track your meds with your symptoms. It sometimes helps to make it more clear that you are herxing, when you see that you changed meds or added meds and then had a flare. VERY TYPICAL!

I'm not a doc.. but in my opinion you just experienced your first herx... which in my case was the hardest. They get easier as your bug load decreases..

I'm sorry you have gone this long with getting no answers... but you may have come across the right answer now.

Keep in touch.. let us know how you are doing!!

--------------------
26 months of treatment. And counting.......

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lou
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There are conflicting opinions about how to handle the herx reaction and you have heard both on this thread. Some say go ahead full blast, high dose, IV. Others say back off on dose or start low and work up.

I think it depends on how serious the herxheimer reaction is, and that is individual. If it becomes intolerable and frightening to the point that you think you might die, well then I think this means you should back off. After all, your bacteria will have been given a field day with immune suppressants, and the load will be high. This is why I would be cautious about the full blast approach early on.

Not a bad idea at all to let your neuro do the Vanderbilt protocol since it would would work for both chlamydia and lyme.

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Michelle M
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Hi Marcstck. I'm sorry you feel so poorly, but I'm glad you found us. Good for you for reaching out and being the master of your own recovery. So many "MS" patients are reluctant to even look into lyme as a possible cause for their illness and are cemented to their diagnosis in a resigned fashion.

I was also dx'd with MS in 2005, with 11 brain lesions and abnormal SSEPS (evoked potentials). However, I'd had a known bite and rash, which my neuro claimed "a reaction to tick saliva" since there's no lyme around here. My spinal tap had no oligoclonal bands (not that that's definitive anyway) but was typical of neuro lyme with elevated proteins.

I was refused a western blot since my ELISA was negative. Subsequent IGeneX was CDC positive and then some! It turned out I also had babesia WA-1 which made for some excruciatingly slow progress.

My neuro had nothing but scorn for my LLMD upon learning I was seeing one. However, it's worth noting that the neuro would have left me to die, in a "wait and see" approach, whereas the LLMD was proactive in getting me better.

Progress was horribly slow, and filled with doubt. It is measured over months -- not weeks or days. Each new med started the herxing process over again with a vengeance!

However, as Sarah said, there is no way out but through.

If you had no infectious process going on, the abx would not much bother you, let alone make you worse. That in itself is of diagnostic value.

I am glad you are seeing Dr. P. I think you are on the right course. Please do keep us posted. There's lots of hope!

Hugs,

Michelle

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TerryK
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Thought you might find this interesting but keep in mind it is not a mainstream journal so it will likely not be credible to your MS doc.



Chronic Lyme borreliosis at the root of multiple s...[Med Hypotheses. 2005] -
PubMed Result

1: Med Hypotheses. 2005;64(3):438-48. Links
Chronic Lyme borreliosis at the root of multiple sclerosis--is a cure with antibiotics attainable?Fritzsche M.
Clinic for Internal and Geographical Medicine, Soodstrasse 13, 8134 Adliswil, Switzerland. [email protected]

Apart from its devastating impact on individuals and their families, multiple sclerosis (MS) creates a huge economic burden for society by mainly afflicting young adults in their most productive years. Although effective strategies for symptom management and disease modifying therapies have evolved, there exists no curative treatment yet. Worldwide, MS prevalence parallels the distribution of the Lyme disease pathogen Borrelia (B.) burgdorferi, and in America and Europe, the birth excesses of those individuals who later in life develop MS exactly mirror the seasonal distributions of Borrelia transmitting Ixodes ticks. In addition to known acute infections, no other disease exhibits equally marked epidemiological clusters by season and locality, nurturing the hope that prevention might ultimately be attainable. As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted. The immunomodulating anti-inflammatory potential of minocycline and hydroxychloroquine may furthermore reduce the Jarisch Herxheimer reaction triggered by decaying Borrelia at treatment initiation. Even in those cases unrelated to B. burgdorferi, minocycline is known for its beneficial effect on several factors considered to be detrimental in MS. Patients receiving a combination of these pharmaceuticals are thus expected to be cured or to have a longer period of remission compared to untreated controls. Although the goal of this rational, cost-effective and potentially curative treatment seems simple enough, the importance of a scientifically sound approach cannot be overemphasised. A randomised, prospective, double blinded trial is necessary in patients from B. burgdorferi endemic areas with established MS and/or Borrelia L-forms in their cerebrospinal fluid, and to yield reasonable significance within due time, the groups must be large enough and preferably taken together in a multi-centre study.

PMID: 15617845 [PubMed - indexed for MEDLINE]

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marcstck
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Just wanted to thank everybody once again for the tremendously helpful information my post generated. I've just posted my Igenix results in another thread, titled "My Igenix Results; Please Help Interpret". Any help you'll give in that regard will be much appreciated...
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treepatrol
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96. Steiner G. 1954 Morphology of spirochaeta myelophthora in multiple sclerosis. Journal of Neuropathology, 13:221-29.P


Four cases of multiple sclerosis, including the case to be reported, elicited abundant numbers of specific spirochetes in the central nervous system to warrant the publication of this paper.


...Morphology and Polymorphism of Spirochaeta Myelophthora: Loops, incomplete, nearly complete or totally complete rings are occasionally seen...


The limited polymorphism of micro-organisms is nothing unusual in microbiology. Especially in old cultures or in chemically and antibiotically treated cases
micro-organisms very often exhibit bizarre forms.
...Classification: ...


What can be said now, with all reservation, is that the spirocheta myelophthora, taken from its morphological appearance in fixed central
nervous system tissues, seems to belong to the genus borrelia of the spirochaetales, family of Treponemataceae.


...Reproduction: ...In multiple sclerosis, as in other chronic spirochetal infectious diseases, there is no continuous reproductive activity of the organisms.


Their propagation may occur at regular or irregular intervals of time....The first fact is the presence of enormous masses of extracellular and intracellular argyrophilic granular bodies in recent plaques of multiple sclerosis.


This is nothing unusual in comparison with other acute or chronic spirochetal diseases, such as relapsing fever and syphilis...


If the granular bodies in multiple sclerosis are developing from broken-up spirochetes, and there is much evidence for it, the possibility of previous presence of countless numbers of
actively multiplying spirochetes in the tissues is not far fetched.


...Transformation: There is a definite sequence of events in the disintegration of the spirochaeta myelophthora. Breaking-up starts with the appearance of loops, rings ,knobs, partial thickening and the formation of granules of different sizes ....Two chronological sequences may be established:


They Know!!


A first phase is the extracellular location of intact, active and probably motile spirochetes, followed by a second phase of extracellular
disintegration in granular form.

The intracellular ingestion of spirochetal debris seems to be a later phase of the pathological process. ...


From here


They Knew in 1954 This is for people Diagnosed with MS or Multiple Sclerosis


For his earlier works, please check the Bibliography file posted at www.lymeinfo.net/lymefiles.html -- they are there, along with quotes from the studies. Some of his colleagues' papers (and rebuttals) are also listed there.


I will post some of the actual text from several papers I have when I get a chance later on.

1950-1965 publications:


STEINER G. [Causes and treatment of multiple sclerosis.]. [German] Munchener Medizinische Wochenschrift. 101:1321-6, 1959 Jul 31.


STEINER G. Comparison of general paresis and multiple sclerosis in regard to the etiological agent. Journal of Neuropathology & Experimental Neurology. 13(3):492-6, 1954 Jul.


STEINER G. Morphology of Spirochaeta myelophthora in multiple sclerosis. Journal of Neuropathology & Experimental Neurology. 13(1):221-9, 1954 Jan.


STEINER G. Acute plaques in multiple sclerosis, their pathogenetic significance and the role of spirochetes as etiological factor. Journal of Neuropathology & Experimental Neurology. 11(4):343-72, 1952 Oct.


STEINER G. Environmental studies in multiple sclerosis. Neurology. 2(3):260-2, 1952 May-Jun.
Currently received at Scott Library; check Library holdings for details.


STEINER G. Experimental allergic encephalomyelitis, spontaneous demyelinating disease and multiple sclerosis. Gazeta Medica Portuguesa. 4(3):824-34, 1951.


STEINER G. Modified silver stain of microorganisms in tissues. American Journal of Clinical Pathology. 20(5):489-90, 1950 May.


STEINER G. Multiple sclerosis. Journal - Michigan State Medical Society. 49(8):938-40, 1950 Aug.


STEINER G. [The study of multiple sclerosis in the U.S.]. [Undetermined] Nervenarzt. 21(11):494-9, 1950 Nov.


Environmental studies in multiple sclerosis.
by Gabriel Steiner, M.D.
Neurology, Vol. 2, May-June:260-262. 1952.


------------------------------------------
``A particular environmental extrahuman reservoir of the disease agent is highly probable.''
------------------------------------------


Environmental studies in multiple sclerosis have been very much neglected. Recent mortality and morbidity statistics (1,2) show that there is a definite geographic difference in the occurrence of this disease.


The present environmental studies are limited to the state of Michigan. Five hundred cases were collected. ...Only cases with well established diagnoses were accepted. ...


The fact that this material of 500 cases comes from two sources, one group examined and evaluated clinically in the Multiple Sclerosis Center and the other group obtained from questionnaire surveys of medical sources is of importance. The results are the same in both groups. ...

1. A difference was found in various regions of the state. ...


2. Intrafamilial cases. In places where multiple sclerosis is more common, there are often more cases in one household. ...


These figures show that in these households females are more exposed to the outside source of the disease than males and that in families, combinations of multiple sclerosis among siblings are two and one-half times more common than paternal-filial combinations.


Apparently sisters and/or brothers are more exposed to the outside source of multiple sclerosis than parents and their sons or daughters.


It seems worthwhile to note that all of the familial cases shared the same household. In one case of two brothers and one case of two sisters the patients shared the same beds for some time before the onset of the disease. Of interest also is the presence of pet animals, dogs and cats, in the same household. Relatively often, these animals were infested with fleas.
'


As to the occupations of the fathers, there seem to be some preferences: farming, gardening and greenhouse work, five times; building industry (lumberman, carpenter, contractor), five times; maintenance of estates (supervisor, janitor), three times; and teaching, three times.


In one of the familial cases (father and daughter) the father had a work shop in the basement of his home.


3. If there is an environmental extrahuman source in our material, other non-familial contact cases should be found also. Of special interest is the case of a girl with multiple sclerosis of two months' duration which was verified by necropsy.


In the home of this girl there was a boarder, a female nurse who took care of a chronic female case of multiple sclerosis in another part of the city. The girl was very fond of cats.


At the time of death of this patient the cat was no longer available because it had to be removed from the home and sacrificed, the reason given was that the cat was flea-ridden.


4. If there is an environmental factor, the occupations of cases may be of interest. In 500 cases of multiple sclerosis collected up to the present, 34 teachers with multiple sclerosis were found. Twenty-five of these teachers were born and teaching in Michigan before the onset of their disease.


It is interesting to note that the disease was found among elementary school and kindergarten teachers 24 times and among high school teachers only seven times. Also interesting is the high frequency of pet animals belonging to teachers.


Cases of multiple sclerosis among non-teaching personnel in schools were found only three times...


There are some of the statistical facts. What are the conclusions?


1. There is no man to man transfer. There is no transovarian passage.


2. A particular environmental extrahuman reservoir of the disease agent is highly probable.


3. This extrahuman reservoir and its accumulation in the environment of certain groups is responsible for the higher incidence in household groups (families) and among teachers, especially kindergarten and elementary school teachers, and moreso in rural areas.


4. In the same household siblings are more exposed to the extrahuman source than in the paternal-filial combination.


5. Dogs or cats may be suspected as reservoirs of the agent. However, the popularity of dogs as pets in the general population renders a statistical evaluation of this factor extremely difficult. Other investigations have been inaugurated.


6. Insect vectors as links in the chain of transmission may be significant or not; the chronicity of the disease and damaged memories in the later stages of the disease make the evaluation of this factor very difficult.


Acute plaques in multiple sclerosis, their pathogenic significance and the role of spirochaetes as etiological factor.
by Gabriel Steiner, M.D.
Journal of Neuropathology, 11:343-72. 1952.


-----------------------------------------------
``In this respect the discovered spirochetes were totally different from the treponema-type and resembled the borrelia-type of spirochetes.''
------------------------------------------------


In the chronic form [of multiple sclerosis] the findings at the time of death represent a terminal cross section of the course of the disease; previous inflammatory reactions may have disappeared partially or entirely.


In many other chronic inflammatory disease entities of the central nervous system and other organs of the human body, acute phases and chronic forms of the same disease entity are of common occurrence.


It is the purpose of this paper to contribute some observations to the study of subacute cases of multiple sclerosis, to discuss some of the pathogenetic features of acute plaques in multiple sclerosis and to establish a relationship between spirochetes and tissue reactions in multiple sclerosis.


...Acute plaques in multiple sclerosis occur, significantly, not only in subacute cases of several months' duration but also in older cases in acute clinical relapse.


Equally and especially important is the presence of older plaques in subacute cases, indicating morphological manifestations dating back to clinically latent initial stages of the disease at its earliest onset.


With these findings in mind, separation of multiple sclerosis into two distinct and different entities seems not justified. [some of Steiner's peers had argued that there were two disease entities -- one an acute disease, the other a purely degenerative chronic disease]


The search for the causative agent in the diseased tissues promises more success when earliest stages of tissue alteration are available for such investigation. Significant pathogenetic information is furnished by the following case of subacute multiple sclerosis.


CASE REPORT


History: A Negro, aged 30 years, was in good health until May of 1948. At that time he noticed weakness of the left leg. This gradually progressed so that he was forced to drag his left leg, and to remain home from work. The paralysis then extended to the left arm and the left side of the face.


His condition grew rapidly worse. Finally he was unable to walk or talk and was admitted to Receiving Hospital on August 7, 1948. ...


Course: The patient improved slightly with supportive therapy until August 20, 1948, when his temperature rose to 102 F. Five days later he developed hyperthermia and fell into a deep coma, without recovery. He expired the following day.


...Post Mortem Findings... Central Nervous System: The entire brain and two small pieces of the spinal cord were obtained...


There were multiple demyelinated plaques in the right parietal region, mostly in the white matter...In the left hemisphere there were a few scattered plaques also...


In sections of the spinal cord no definite plaques were found but some whitish discolorations in wedge shape with the base at the periphery.


Microscopic Observations: In myelin sheath preparations, numerous demyelinated plaques were seen (fig. 1). In these plaques the myelin sheaths were either completely lost or a few islands of preserved myelin sheaths were seen, but the complete loss prevailed.


The demyelinated plaques were of varying dimensions. In fat stains these demyelinated areas showed equal distribution of the fatty products;


in older plaques, however, these fatty products were lacking or remained in larger quantities only in adventitial spaces of blood vessels. ... The nerve cells in plaques were well preserved (Nissl stain). ...


When grey and white matter participated in one single demyelinated plaque the demyelination took place in grey and white matter alike without respect to the border-line between grey and white matter. ...


The Special Silver Salt Reduction Technique to Demonstrate Granular Bodies and Spirochetes:
[a detailed description is provided].


Extracellular Granular Bodies: These granules were of varying sizes and shapes. Round, ovoid, or irregularly contoured shapes were common. ...


Two or more granules in close proximity were also seen. The dimensions of these extracellular granules varied from the size of a mast cell granule to one of the size of a red blood corpuscle or even of a small glial nucleus.


Often the extracellular granules and astrocytes containing intracellular granules were accumulated around blood vessels in perivascular parenchyma.


They were seen abundantly also in the parenchyma without any relationship to blood vessels and less frequently in vessel walls themselves. The photomicrographs (fig. 4)


show better than any detailed description the shapes, sizes and locations of these extracellular granular bodies.
[a series of photographs of spirochetes and spirochetal granules found in the autopsied tissues is provided]


Intracellular Granular Bodies: ...The granules differed in shape and size from the extracellular granules. They were more massive, and of a very irregular shape.


Nevertheless, they were of the same black, shiny color. ...The intracellular granules were demonstrable by the silver techniques I and II.


Spirochetes: In their fully developed, not yet disintegrating forms, the spirochetes appeared as screw-like organisms. ...Crests and roots were always rounded, never pointed.


The minimal thread angle was 60, its maximum 130, the average being 97. In this respect the discovered spirochetes were totally different from the treponema-type and resembled the borrelia-type of spirochetes. ...


Knobs at one end were not unusual (figs. 8d, e, and 9c). There were also loops in the center of the longitudinal axis or more toward the end. The spirochetes were completely detached from any tissue elements. ...


The spirochetes were found in marginal areas of acute plaques and in perifocal location in areas close to the periphery of acute plaques, often in histologically seemingly intact tissues. They were always found in locations where abundant extracellular and intracellular granular bodies were present.


This close spatial relationship between the spirochetes and the granular bodies is of the greatest practical importance in finding intact and well preserved spirochetes. When masses of extracellular and intracellular granular bodies are found, spirochetes should be looked for at the peripheral areas of an acute plaque containing granular masses close to and in the normal tissues of the central nervous system.


One should not expect, however, to find such enormous masses of well preserved spirochetes, as for example, treponemas are seen in the organs of congenital syphilis...


The highest number of individual spirochetes in brain and spinal cord of this polysclerotic case were 8 in a high power oil immersion microscopic field. ...


The not disintegrated spirochetes [8 were found] apparently represent stragglers left behind by an enormous army of regularly coiled individual spirochetes.


If the granular bodies seen in abundant masses are remnants of disintegrated spirochetes these microorganisms must have been present in enormous numbers and apparently their individual life-span must have been short, in inverse ratio to the speed of reproduction.


Excessive reproductive activity of spirochetes, that is speed of multiplication on one hand and very short life-span of the individual spirochetes on the other, are conclusions to be made from the histological appearances.


Significance of Granular Bodies: The very abundant accumulation of granular bodies in close regional relationship to polysclerotic plaques of acute or subacute order can easily be detected. Thus, the granular bodies were seen by many observers (Austregesilo (son) (11), Steinger (12), Guirand (13a, b), Rogers (14), Austregesilo (father) and Fortes (15), Scheinker (16a,b), Marburg (17).


These granular bodies were interpreted differently by the various observers, but all agreed that they represented products of disintegration either of tissue elements (Marburg (17)) or of microorganisms. Only Giraud (13a,b) claims that the bodies are the microorganisms themselves. ...


The Relationship of Granular Bodies and Spirochetes: There are all intermediate stages between well preserved regularly coiled spirochetes and granular bodies. There are terminal granules with adherent spirochetal threads (fig. 9c); there are granules already freed from the still persisting spirochetal thread, but at a very short distance from it,


so that the breaking off of the granule from the spirochetal thread seems very probable. ...There are spirochetes...still showing the structural continuity between the granule and the spirochete.


The knobs and loops represent probably the earliest transitional phases from the spirochetal form to granule formation. There is no doubt that the granular bodies, the haptocytes and the spirochetes are in intimate pathogenetic relationship. ...


The biological significance of these bodies in multiple sclerosis is still obscure. One aspect, however, is certain: These granular bodies are definitely related to the presence of well preserved spirochetes and their disintegrating forms.


Granular bodies in general may represent 1) involutional forms (a) with possibility of redevelopment into typical spirochetal forms, (b) representing beginning disintegration and final death of the spirochetes,


(c) possibility of (a) and (b), that is, redevelopment into spirochetal forms as well as irreversible disintegration; 2) specific evolutional forms in the life-cycle of the spirochete. At present no decision between 1) or 2) is possible. ...


Experimentally we can produce the granular bodies in cultures of well known spirochetes by exposure to a temperature to 56 centigrade. ...


In the case of multiple sclerosis it is certainly premature to speculate about the significance of the granular bodies in the life cycle of the specific spirochetes.


Nevertheless, the value of the granular bodies as indicators of spirochetal presence in the tissues cannot be underestimated.


In Table I a short review of positive findings [of spirochetes or granules in cases of multiple sclerosis] has been compiled. ...


Until 1936, among 48 examined cases of multiple sclerosis, 12 were spirochete-positive (25 per cent). Two of these 12 cases (Brack and Kocheise) showed numerous spirochetes. Silver cells were found in over 90 per cent of the examined cases and haptocytes in 25 per cent. ...


In old chronic and treated cases of general paresis spirochetes are never found and the same is true for old stationary cases of tabes dorsalis.


It is well known to the pathologist that the microscopic search for the agent in chronic infections, such as tuberculosis and syphilis is often troublesome and does not succeed. Why should it be different in multiple sclerosis?


EVIDENCE OF SPIROCHETAL NATURE


1. The specific morphology of the spirochetes could be described, photographed, and measured. The spirochetes were seen in large numbers in 4 cases of multiple sclerosis in identical morphology. Nothing like it was found in numerous control cases.


2. The order of magnitude is that of spirochetal organisms. The spirochetal structures are of varying length, from 4-18 microns. Their cross section is round like in all spirochetes.


Length, thickness and shape of the spirochetal structures vary in the same range as in other well-known spirochetes.


There are, however, enough specific morphologic peculiarities of these spirochetes which distinguish these organisms from other known spirochetes.


3. The staining reactions were the same as shown by other well known spirochetes contained in tissues.


The typical silver affinity of all well known spirochetes which is essential for the demonstration of every type of spirochetes in tissues is a definite quality of the spirochetal structures in cases of multiple sclerosis. The specific argyrophilia of the spirochetal surface is common to bacterial surfaces but not to protozoan surfaces.


All these bacterial and spirochetal organisms are without the colloidal protection against the silver mirror formation or at least without the same protection as most tissue elements and protozoa possess. That is the reason why tissue structures stain in yellow tinges while bacteria and spirochetes take the metallic mirror-like black silver coating.


There is also a difference between the surface of bacterial rods and cocci, as well as of fungi on the one hand and that of spirochetes on the other, insofar as most bacteria and fungi need less time of exposure to silver salts (silver nitrate) to be reduced to metallic silver.


A difference between the surfaces of bacterial and spirochetal organisms seems also to be indicated by the fact that the color reaction in living bacterial cultures by reduction of colorless tetrazolium salts (see article of Smith (39)) is quite common while living leptospira cultures at our disposal did not change their natural color into blue or red.


4. The spirochetal structures are completely detached from any tissue elements at both ends as well as on all sides.

They appear as foreign bodies in the tissues. Very often an empty space or microvacuole is surrounding the black, mirror-like structure of the spirochete.


5. The spirochetes are seen in the parenchyma of brain and spinal cord itself, as well as in the vascular walls. This also excludes the possibility that these spirochetal structures may be elements of the parenchyma proper or reticular fibrils of the vascular walls.


To the eye of the experienced microscopist the reported structures cannot be explained otherwise than as specific spirochetes. They differ from any other known type of spirochetes, especially from the treponemas or leptospiras.


They resemble the species of the Borrelia group of spirochetes. I named the organisms spirocheta myelophthora, that is, the myelin sheath destroying spirochete.


HOW TO FIND THE SPIROCHETES


The spatial and temporal conditions for a successful search for spirochetes have to be considered first. Not every polysclerotic plaque contains spirochetes.


Old plaques with only little inflammatory reactions are unfit for the search. Plaques containing massive amounts of catabolic neutral fat are already too far advanced in the disease process to show spirochetes. ...the normal tissue between two neighboring acute plaques is a good place to look for spirochetes.


The examination for spirochetes in silver preparations is greatly facilitated by the presence of extracellular and intracellular (in astrocytes and microglia cells) granular bodies in masses.


Extracellular granules seem to be the first manifestations of spirochetal disintegration. A later phase in intracellular. The finding of extracellular granular bodies is the first step for the search of spirochetes. ...


The best preserved spirochetes were found at the margins of an area containing the granular bodies in masses and always at the margins of such a field toward the normal tissues and not toward the inside of a demyelinated plaque.


...Compared to the immense masses of granular bodies, spirochetes are less frequently found. The well preserved remaining spirochetes are to be considered, as already mentioned, as stragglers...


...The search for spirochetes in advanced, non- or slowly progressing cases is too tiresome and time consuming to promise a good chance for finding spirochetes.


...There remains the problems of who should look for these organisms. Diligence and patience of the examiner and ample time at his disposal are necessary requirements.


The investigator should be acquainted with the various silver stains used for demonstration of tissue elements of human body and especially of the nervous system such as neurofibrils, neuroglia cells etc.


Some knowledge of the appearance of spirochetes in tissue sections of the central nervous system and other organs of the body prepared with silver techniques will easily be acquired.

POSSIBLE SOURCES OF ERROR


1. Do the spirochete-like structures reported herewith represent pathological or normal tissue elements of the central nervous system and have nothing to do with multiple sclerosis?


No structures similar to or identical with the spirochetes have been found in over 250 control cases of diversified diseases other than multiple sclerosis and of normal brains. ...


the regularity in form and shape, the limitations at both ends of positive spirochetal findings exclude a mistaken interpretation as argyrophilic senile filaments. ...


2. Artifacts. In one textbook of neurology the spirochetal structures found in multiple sclerosis have been considered as artifacts (Grinker and Bucy (42)).


...Control sections of tissues containing numerous known spirochetes... were used in each batch of staining procedures. These sections serve at the same time as controls for the blackness of the silver-mirror on the spirochetes.


Those who regard the spirochetal structures as artifacts are without experience in staining techniques of spirochetes or in the appearance of spirochetes in stained tissue sections. ...


To assure a wide range of control of artifacts, numerous pieces of tissue from normal brains or from those affected by diversified diseases were exposed to autolysis, then fixed in formalin, embedded, cut and stained in the same way.


No structures like those seen in brains and spinal cords of cases of multiple sclerosis were found. ...


3. The disclosed spirochetes cannot be those of syphilis, post mortem invaders, secondary invaders or contaminants. Spirochetes are found in normal man in the mouth, in the respiratory tract, in human feces and in genital regions.


They are, for the most part, harmless non-pathogenic commensals. Spirochetes were never found in the central nervous system of normal man.


...[in] the case presented here and previous cases of multiple sclerosis in which spirochetes were found (Steiner (18, c, d, e), (Rogers (14), Austregesilo and Fortes (15), Scheinker (16)) syphilis could be excluded.


Moreover, the disclosed spirochetes do not resemble at all the treponema pallidum; they are specific spirochetes, possibly belonging to the borrelia group


It is known that in the terminal phase of life, the last hours before death and after death central nervous system tissues can be invaded by saprophytic micro-organisms. ...


The characteristic and typical finding in such cases is the lack of all inflammatory tissue reactions in spite of the presence of masses of bacteria. On the other hand,


in multiple sclerosis there are often massive inflammatory reactions at the borders of recent demyelinated plaques, inside of these and their near extrafocal vicinity. These inflammatory reactions are only indirect evidence of past and present activity of the agent.


The immediate proof of its activity is its presence in forms of varying stages of well preserved to disintegrating forms, from regular spirochetal forms, more or less straight forms to all types of granular spirochetal disintegration, extra- and intracellularly.


Particularly, the intracellular astrocytic and microglial ingestion of granular bodies is proof of the intravital activity of the disease process and its agents. Nothing like it is seen in other diseases when secondary post mortem invasion has taken place. ...


4. The possibility that the disclosed spirochetes are harmless intravital saprophytes must be excluded also. The histological reactions are evidence of tissue damage and besides no visible microbial saprophytes have ever been found in brains of normal or diseased human beings. ...


5. Another possibility has to be considered: that is the presence of the spirocheta myelophthora as a microscopically visible and detectable agent together with an ultravisible viral agent. This eventuality cannot be ruled out by our morphological studies with the light microscope.


However, such a possibility does not detract anything from the etiological and pathogenetic significance of the findings of spirochetes. In principle, it seems to me very precarious to conclude from our inability to find visible organisms that the agent must be a virus.


We know at least one spirochetal infectious disease which was considered due to a virus until Gsell (44) established, beyond doubt, its spirochetal origin (Leptospirosis pomona).


6. A personal error in interpretation of the findings has also to be excluded. ...The slides containing spirochetes were shown to Drs. Brines, Olsen, Weller, Wohlwill and Zimmerman. In critical appraisal they all acknowledged the shown structures as spirochetes of a type different from treponema pallidum.


As an argument against the spirochetal findings and their significance it has been said that reproduction of the same findings by others is lacking.


In fact, it is shown in Table I that among a total of 31 cases examined by various investigators 11 showed spirochetes (over 35 per cent). Thus, the demonstration of specific spirochetes has been possible in more cases of multiple sclerosis and by other investigators.


I, myself, was able to find the spirochetes in considerable numbers in 4 cases (once in brain and particularly in spinal cord, once in a case with a second acute relapse after 12 1/2 years remission, once in a case with miliary granulomas, the fourth case is being reported herein).


In cases of chronic type the finding of spirochetes is too sporadic to spend much time and effort. Rogers (14), using Marburg's material in Vienna, found the spirochetes in 1 among 11 cases.


Blackman (20) found structures resembling spirochetes in 5 of 11 cases of multiple sclerosis. Scheinker (16b) saw spirochetes in 4 out of 8 examined cases. Austregesilo and Fortes reported 1 positive case of a 38 year old woman with a duration of 8 months of disease. ...


Spirochetes cannot be expected to be seen in every case of multiple sclerosis. The best chance for finding the spirochetes is in polysymptomatic cases of short duration (3 to 8 months) or older cases in recent relapses. Old burned-out cases do not offer much chance. ...


Without the use of adequate silver methods and without a diligent search a reproduction of my findings is impossible. The time applied for the search is proportional to the success of finding spirochetes. ...

A great number of problems are still unsolved:


How do the spirochetes enter the human body? After the entry of the organisms into the body are there systemic reactions or not?


How much time elapses from entry into the body until the organisms reach the central nervous system? Where do the spirochetes harbor in the clinically latent initial phase of the disease? And where do they reproduce?


What is the stimulus for a new reproductive phase of spirochetes responsible for relapses and acute exacerbations? ... Are there immunological reactions to the presence of spirochetes in the body?


... A special problem arises when we consider the pathogenic role of the spirochetes and the granular bodies, derived from the spirochetes. Is the activity of motion of these corkscrew-like organisms the essential tissue damaging and myelin-sheath destroying factor?


In other words, is a micromechanical injury the real tissue damaging effect? Or are substances of the spirochetes or derivatives of these, for example the granular bodies and their substances biochemically noxious myelolytic agents?


Or is the defense reaction of the central nervous system itself, especially astrocytic proliferation and haptocyte formation more harmful and injurious to the tissues, particularly to the very sensitive myelin sheaths than the spirochetes themselves and their granular bodies?


In multiple sclerosis the detectable tissue damage may be tardy in its development and quite some time behind the appearance of actively motile spirochetes and their granular bodies.


These visible tissue reactions may appear some time after the spirochetes and their granular bodies for the most part have already disappeared. This would not be unusual when compared with other chronic infectious diseases.


It could explain also the difficulties in detecting the causative agents in the majority of chronic cases and the good chance of finding the spirochetes in subacute cases or in acute relapses of older cases.


With a new discovery a great number of new problems arise and new ways of investigation will lead to new endeavors which may successfully solve the overall important therapeutic problem of multiple sclerosis.


Morphology of spirochaeta myelophthora in multiple sclerosis.
by Gabriel Steiner, M.D.
Journal of Neuropathology, 13:221-29. 1954.


--------------------------------------------
``What can be said now, with all reservation, is that the spirocheta myelophthora, taken from its morphological appearance in fixed central nervous system tissues, seems to belong to the genus borrelia of the spirochaetales, family of Treponemataceae.''
------------------------------------------------

In a recent paper (1) the findings of specific spirochetes in the brain of a newly examine subacute case of multiple sclerosis were reported and evaluated.


The purpose of the present paper is to give a detailed description of these spirochetes, their classification, their reproduction, and disintegration.


Four cases of multiple sclerosis, including the case to be reported, elicited abundant numbers of specific spirochetes in the central nervous system to warrant the publication of this paper.


1. Further Evidence of Spirochetal Nature: It has been said that the reported spirochetes represent only spirochete-like structures of the tissue proper, such as reticulin fibrils, neurofibrils, or axis cylinders.


To disprove these objections the following experiments were done: [detailed description given]...This [the results of these experiments] is definite proof that the ``spirochete-like structures'' are not related in any way to fibrillar reticulin elements, neurofibrils, or axis cylinders. ...

2. Morphology and Polymorphism of Spirochaeta Myelophthora: [detailed description given, as well as photographs for supporting evidence] ...


Most characteristic is the corkscrew-like regularly coiled form with 5 to 12 single shallow spirals and with always rounded, never pointed, crests and roots.... the hook at the end shows a round, arc-like bending and is entirely different from the characteristic whip-like ends of the leptospiras.


Loops, incomplete, nearly complete or totally complete rings are occasionally seen... The limited polymorphism of micro-organisms is nothing unusual in microbiology. Especially in old cultures or in chemically and antibiotically treated cases micro-organisms very often exhibit bizarre forms.


3. Classification: The classification of spirochaetales is still not very satisfactory. Up to the present time 3 genera are recognized... treponema, borrelia and leptospira...


What can be said now, with all reservation, is that the spirocheta myelophthora, taken from its morphological appearance in fixed central nervous system tissues, seems to belong to the genus borrelia of the spirochaetales, family of Treponemataceae.


4. Reproduction: ...In multiple sclerosis, as in other chronic spirochetal infectious diseases, there is no continuous reproductive activity of the organisms. Their propagation may occur at regular or irregular intervals of time.

...the facts concerning the morphological identification must be properly evaluated so that mistakes can be avoided as much as possible. ...


The first fact is the presence of enormous masses of extracellular and intracellular argyrophilic granular bodies in recent plaques of multiple sclerosis. This is nothing unusual in comparison with other acute or chronic spirochetal diseases, such as relapsing fever and syphilis...


If the granular bodies in multiple sclerosis are developing from broken-up spirochetes, and there is much evidence for it, the possibility of previous presence of countless numbers of actively multiplying spirochetes in the tissues is not far fetched.


...There is not the least evidence for an intracellular reproductive activity of spirochetes in the nerve cells or other cells of the human tissue. The cells are not even used as shelters by the spirochetes. This is in accordance with the behavior of other classified spirochetes.


In multiple sclerosis the spirochetes are located only in extracellular regions of the cerebral and spinal cord tissues. The process of individual growth and reproduction does not involve any intracellular phase and is exclusively extracellular.


...The question also arises as to whether or not permanent inactive forms, such as spores, do exist.... no morphological facts favor such as theory. The granular bodies, as in other spirochetal organisms, represent in all probability, remnants of disintegrated spirochetes.


Many attempts to establish an evolutional cycle of the granular bodies into spirochetal forms in many other well known spirochetal genera have failed to demonstrate convincing evidence.

5. Disintegration: There is a definite sequence of events in the disintegration of the spirochaeta myelophthora.


Breaking-up starts with the appearance of loops, rings (fig. 2d), knobs, (fig. 1r, s, t), partial thickening and the formation of granules of different sizes ....


Two chronological sequences may be established: a first phase is the extracellular location of intact, active and probably motile spirochetes, followed by a second phase of extracellular disintegration in granular form.


The intracellular ingestion of spirochetal debris seems to be a later phase of the pathological process.
...It should be mentioned here that the disintegration of the spirochaeta myelophthora proceeds in the tissue rather rapidly.


In all our cases tissue blocks, containing abundant numbers of spirochetes, were less numerous than blocks containing extracellular and intracellular spirochetal debris without spirochetes. In old plaques, there is no chance to find argyrophilic granules or intact spirochetes.

6. Pathogenesis...: ...The heterophasic nature of the disease process should be, however, emphasized.



It is characterized by the presence of histologically old, more recent and of fresh plaques; the variation of inflammatory reactions in relation to the stage of the plaque and the number of well preserved spirochetes and extracellular spirochetal granular debris in or near acute plaques is impressive.

A detailed histopathogenetic analysis is still a postulate of the future. The spirochetes appear in complete detachment from any tissue element proper, often surrounded by a small halo.

This micro-halo has been mentioned by several observers concerning the appearance of treponema pallidum in stained sections of the central nervous system.


In some of my sections the spirochetes were surrounded by a definite microscopic vacuole in which no tissue elements were found (fig. 1t). This may or may not indicate a tissue-liquefying power of the spirochetes. ...


95. Czekalowki JW; 1954 Formation of granular structures by Leptospirae as revealed by the electron microscope. Journal of Bacteriology,67:619-627.R Eaves G.P


Leptospira began to show granulation after 2 weeks in a culture. The granules were spaced regularly within the bodies of the spirochetes. After four weeks larger type of granule appeared which was broader than the body of the spirochetes.


These were later "shed free." By the 5th to 7th month, there were no
spirochetes observed; the culture contained only granules. The granules consisted of "what appears to be short segments of leptospiral body embedded in homogeneous substance.

The authors conclude that the formation of granules represents a rhythmic and constant process and hence these granules must
play a role in the life-cycle of leptospirae.

Theres another spirochete.

46. MacDonald AB. 1988 Concurrent neocortical borreliosis and Alzheimer's disease: Demonstration of a Annals of the New York Academy of Sciences,
spirochetal cyst form. 539:468-470.

Page IV In vivo finding of Borrelia burgdorferi cysts in an autopsy of a human brain. An unexpected observation was the identification of cystic forms of the Borrelia
spirochete in dark-field preparations of cultured hippocampus, and in imprints of hippocampus...


A cystic form of the Borrelia spirochete would explain the ability of the microbe to persist in the host during a prolonged period of asymptomatic clinical latency, which spans the period between primary infection and
the expression of tertiary manifestations of neuroborreliosis.


Zajkowska JM; 2002 New aspects of the pathogenesis of Lyme disease. Przegl Epidemiol, 56 Suppl 1:57-67.
Hermanowska-
Szpakowicz T.

From the abstract: Morphological changes of B. burgdorferi as well as changes in expression of surface proteins caused by environmental determinants are essential in pathogenesis of Lyme disease.


Cysts, spherical form spheroplasts, L-form and `blebs' gemmae can be responsible for long lasting antigenic stimulation, signs of chronic borreliosis, and even probably connected with MS and Alzheimer disease.


Go to link and get on abx and anti parasitic drigs a good LLMD will treat you for all.

--------------------
Do unto others as you would have them do unto you.
Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.

Newbie Links

Posts: 10564 | From PA Where the Creeks are Red | Registered: Jun 2003  |  IP: Logged | Report this post to a Moderator
pattilynn
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Member # 8065

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I also started the Vanderbilt protocol one month ago. I added doxy yesterday. I have numerous neurologic symptoms with all normal testing and a history of bullseye rashes. My WB was negative. Igenex IGM 39 IND, 41 IND, 30+. My burning sensations have returned.
Posts: 340 | From Ohio | Registered: Oct 2005  |  IP: Logged | Report this post to a Moderator
Monica
Frequent Contributor (1K+ posts)
Member # 224

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I am very sorry to hear about your condition. My story is not dissimilar.

Won't go into all the details, but believe I have been infected for 19 years.

No abx till 1997. Among other symptoms I developed a weakness in my right leg.

I was on and off low dose oral abx till 2002 at which time I had 2 1/2 months of IV rocephin. Had I continued I believe I would have seen the leg weakness completely disappear as that was the best I felt in this century!

In 2003 I was off all abx and worked in an extremely stressful environment. My condition rapidly went downhill.

In 2004 back on low dose oral abx.

In 2005 I saw, for the first time, an alleged LLMD. My Igenex test came back positive for Lyme only. He put me on mega antibiotics. I went into his office using a cane, and a year later I was in a wheelchair. He kept telling me I was herxing, that I had to get worse before I got better. The truth was I was rapidly deteriorating.

Once off the abx in July 2006 my condition stabilized. I am still wheelchair bound, but no worse and I am seeing some improvements in my leg and foot movements.

I am under the care of another LLMD and am currently seeing a new neurologist who has ordered new MRIs for me. Haven't had an MRI of the spine in 7 years so I will be very interested to see what that shows. MRI of brain a year ago showed multiple "abnormalities."

I hope my story is of some use to you. Please feel free to PM me if I can provide you with further info.

Posts: 1757 | From Somerset County, NJ | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
   

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