Can lyme mimic ALS?

yes please research the dr david martz story . his apprentices practice in colorado may accept new patients . also band 41 is presence of flagella detected . very few bacteria have flagella namely spirochetes.

here is dr c exp of band copypasta from lymenet flash. i had to do a year of pulsed iv rocephin with the als/ms misdiagnoses to gain my mobility back . remember als means it already has done nerve damage so one cannot do treatment so fast as to cause more damage with lps dieoff and herxheimer effects are not for the faint of heart.

"The following is a brief explanation of the test results. Again, each band is an antigen complexed (bound together) with an antibody made by the immune system, specifically for that antigen (part) of Borrelia burgdorferi.

18: An outer surface protein.

22: Possibly a variant of outer surface protein C.

23-25: Outer surface protein C (osp C).

28: An outer surface protein.

30: Possibly a variant of outer surface protein A.

31: Outer surface protein A (osp A). 34: Outer surface protein B (osp B).

37: Unknown, but it is in the medical literature that it is a borrelia-associated antibody. Other labs consider it significant.

39: Unknown what this antigen is, but based on research at the National Institute of Health (NIH), other Borrelia (such as Borrelia recurrentis that causes relapsing fever), do not even have the genetics to code for the 39 kDa antigen, much less produce it. It is the most specific antibody for borreliosis of all.

41: Flagella or tail. This is how Borrelia burgdorferi moves around, by moving the flagella. Many bacteria have flagella. This is the most common borreliosis antibody.

45: Heat shock protein. This helps the bacteria survive fever. The only bacteria in the world that does not have heat shock proteins is Treponema pallidum, the cause of syphilis.

58: Heat shock protein.

66: Heat shock protein. This is the second most common borrelia antibody.

73: Heat shock protein.

83: This is the DNA or genetic material of Borrelia burgdorferi. It is the same thing as the 93, based upon the medical literature. But laboratories vary in assigning significance to the 83 versus the 93.

93: The DNA or genetic material of Borrelia burgdorferi.

In my clinical experience, if a patient has symptoms suspicious for borreliosis, and has one or more of the following bands, there is a very high probability the patient has borreliosis"

Symptoms overlap, but in ALS there is lung "gurgling".

Ive never heard of that with lyme. Air hunger, yes, fluid in lungs? no. (I could be wrong)

lasjps said...
My husband was diagnosed with ALS in October 2022. It started with foot drop in his left foot. He was tested with Western blot test which was negative. He has progressively gotten weaker with muscle atrophy and is mostly wheelchair bound now. We recently had the Igenex test, and he tested positive for the following bands:

IgM - 23+ and 41+
IgG - 31++ and 41+; 23 IND

We have not seen a doctor yet, but are in NE PA. We are scheduled to see an Infectious Disease doctor in a week, but also feel an LLMD would be the best. Just having a hard time locating/deciding.

Please let me know if you have any insights for us!! Thank you.

I've heard other people say they were misdiagnosed with ALS bt really turned out to be lyme. As for nerve damage and getting muscles and nerve damage under control, what I took for that was vitamin b1 (the real form of it) Dr. Berg website has it or another real brand if you can find it. Also nutritional yeast flakes are packed with vit b for nerve damage. We gave some to my bfs father who has diabetes and nerve damage and he said he feels great. Prior, he was weak, had issues walking without a walker, seeing, thinking , driving the car etc.

I just read this over on lymenet.org

https://www.mdpi.com/2079-6382/12/6/1021

Abstract

This study aimed to demonstrate that severe neurological motor deficits in the context of late tick-borne disease with mixed microorganism involvement are eligible for long-term combined antibiotic/antiparasitic treatments. The inclusion criteria were: 1. neurological limb paralysis with a disability score >4 according to the EDSS Kurtzke disability scale; 2. serological tests pointing to an involvement of the main tick-borne microorganisms Borrelia burgdorferi s.l., Babesia, Anaplasma, and Bartonella; 3. a general disease for more than 6 months with fatigue, pain and subjective cognitive deficit. The patients were administered long-term treatments with repeated cycles (at least three) of 35-day IV ceftriaxone and repeated oral regimens of azithromycin–doxycycline and azithromycin–doxycycline–rifampicin. For Babesia, repeated courses of atovaquone–azithromycin were administered. Ten patients had intractable or severe motor deficits before treatment in the context of Borrelia (two cases) Borrelia–Babesia (four cases), Borrelia–Babesia–Anaplasma (two cases), Borrelia–Babesia–Anaplasma–Bartonella (one case) and Babesia–Anaplasma (one case). For several months, five had been in wheelchairs, and four had been walking with sticks. Seven patients out of 10 (70%) showed complete remission after a mean active treatment duration of 20.1 + 6.6 months, with a mean number of 4 ceftriaxone cycles. Three patients showed an initial remission but suffered secondary antibiotic/antiparasitic-resistant motor recurrences. Among the nine patients with Borrelia serologic positivity, treatments obtained complete remission in seven cases (77%). The findings of this ten-case series suggest the usefulness of long-term antibiotic/antiparasitic treatments in patients with severe late tick-borne neurological deficits with highly significant elements of tick-borne involvement.