Re: New here questions on lyme and other

On Feb 18, 10:19 pm, cowabungabartnewsgrouplea...@xxxxxxxxx wrote:
On Feb 18, 11:30 pm, Needsomeinput <needrealhel...@xxxxxxxxx> wrote:

On Feb 18, 7:21 pm, cowabungabartnewsgrouplea...@xxxxxxxxx wrote:> On Feb 18, 7:57�pm, Needsomeinput <needrealhel...@xxxxxxxxx> wrote:

Hi Cowabunga


Well h pylori can cause a lot of problems and be very refractory to
treatment.

Sure that was the case for my sister


Not all symptoms are ulcer like. Some patients can be asymptomatic and
others have gi problems but not ulcer symptoms for example gastritis
is common. H pylori has even been linked to certain cancers..

http://www.cancer.gov/cancertopics/fact***/HPylori

and also autoimmune conditions (the most obvious is in fact
gastritis), FYI I didn't have gastritis according to the endoscopy

as you probably known is somewhat of ubiquitous, but
I went ahead and took the antibiotics for that (long course) and I
didn't took any probiotics. At any rate the next 2 days after the
final dose I came extremely ill an had to go on short term disability
from work. Is hard for me to believe that if it was indeed Lyme you
would have such a rapid and acute onset of neuro symptoms.

Not sure why you would doubt that? Some patients have frank fulminant
meningitis within days or weeks of initial tickbite and infection.

But not 2 days after a 7 days of H pylori treatment that included a
combo of antibiotics (amoxicilin and Clarithromycin)


Also you don't really know time of infection do you since you don't
recall a tick bite? Lyme can lay dormant or latent like syphylis. You
might have had a mild apparently self limited summer flu which
ultimately turned into full blown neurological involvement from Lyme.
Maybe you even were given some short course of antibiotics, which, by
the way can abrogate the immune response and render patients
seronegative once and forever. see Dattwyler RJ, Volkman DJ, Luft BJ,
Halperin JJ, Thomas J, Golightly MG. Seronegative late Lyme
borreliosis: dissociation of specific T- and B-lymphocyte
responses to Borrelia burgdorferi. N Engl J Med 1988;319:1441-1446.
[Abstract]

Unfortunately since I'm out of work I don't have access to the full
document from my home and just from the abstract is hard to make any
educated comment. However, this article is from 20 years ago (a few
years later after HIV was discovered and in theory about the same time
by which a vaccine would be developed), I guess I don't need to say
how 20 years can affect knowledge and methodology in many scientific
fields. I'm not saying that the observations are not valid but if you
have a more recent article that corroborates their findings I would be
more compelled to believe it. I'm pretty much certain they didn't
define chronic lyme disease based on any culture of the pathogen (I
know is hard but it can be done an only those patients should be
included) in other words they assume there was Borrellia in their
systems based on their symptoms and previous history, further more all
the testing against antibody response were negative further supporting
that these individuals could may as well have cleared the infection
completely. They make a weak case on chronic infection based on
results of T-cells response, which have been observed (of course) in
patients with inflammatory processes (autoimmune). Do you a have
reference for "Although prompt treatment with antibiotics may abrogate
the antibody response to the infection, symptoms persist in some
patients" since they put it forward as a matter of fact in the
abstract they should have a reference for it in the complete article.


Well honestly depending on how long standing your case is, IF it is
Lyme, a month of rocephin is not all that likely to make a dramatic
difference particularly if you have real CNS involvment. Sort of like
spitting on a forest fire through a mesh screen if you will (blood
brain barrier).

Really, wouldn't you expect some effects quickly on I.V.?

Again not necessarily. Sometimes you might see a worsening of symptoms
shortly after treatment particularly using rocephin a bacteriacidal
drug, as you most likely know this is called a jarisch herxheimer like
response seen in syphylis, relapsing fevers and lyme disease (though
having spent time on Lymenut you and having a scientific background
and ability to research AND understand what you read, you probably
realize that the J-H like response seen in Lyme is NOT what people
think it is on lymenut where people attribute what are most likely
side effects of medications and fluctuations in symptoms with

"the J-H
like response which can be quite severe but is relatively short lived
and happens almost immediately following treatment."

exactly, almost immediately following treatment, and i.e patients with
syphilis that were the most acutely ill would be the ones more likely
to suffer from this reaction, since the load of the pathogen is
associated with the degree of illness and the more toxins are released
the less likely the body would be able to cope with it, thus J_H
reaction. In my case I was acutely ill however didn't experience an
J_H reaction at all (again using I.V rocephin).


I could
understand the hypothesis that a month will not cure it but I would
expect changes even within days. What would make it "able" to work
beyond say 1 month, if your body is constantly metabolizing the
antibiotic?

Again there are many theories. Start with long reproduction time of
the bacteria recalling the mechanism of action of antibiotics.

That doesn't answer the question, it only points out why is possible
that lyme could be refractory and in general why in any bacterial
infection specially those with slow reproducing cycles is important to
complete the antibiotic protocol to assure eradication of the
pathogen. As you know people are warned by their Drs specifically
since they feel so good only after a day or 2 of antibiotics (i.e H
pyloris) to not discontinue the treatment.

Follow it by pleomorphic forms, cell wall deficient forms, sequestered
locations, the apparent ability of the bacteria to essentially
sporulate in the face of hostile environements...

again unrelated, only pointing out the fact that it can be remain
latent and the patient my relapse..

Honestly there are many theories none very well established and
documented but many with at least some evidence to support these
theories.

For what I specific ask, I think there is only anecdotal evidence
(usually from the same people that when having an anaphylactic shock
blame it on a herx reaction).


A good article (full text) if you missed it can be found at:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubme....

thanks for the article

still working on it..(interesting but so far not really answering my
more urging concerns)

I think it is worth a read and then return to discuss since it
explicates very well (and better than I can if you can understand the
jargon which I am confident that you can.


many people are and worse than me. I've improved greatly from my
sickest but it took a long time and a lot of treatment a lot of ups
and downs along the way.

Nice to hear, there is hope


In all honesty I think Igenex testing is B.S, well maybe
now they are stricter on what they do and their tests are just the
same as any other big lab (Quest) that is after they were investigated
and asked to change their practices (at the end I just think that
Harris was trying to make money in a very irresponsible way). I
thought that the babesia test was something less of an issue and that
I could actually get an accurate result (that's what it was ordered
together with the lyme test).

I can't really take a firm position on the validity of igenex testing.
Let's say that there has been grounds for suspicion. But I'm not in a
position to validate or invalidate the testing.

Well I do take a position when I know that Harris managed himself in
such an unprofessional way lying to the public and the media. I
personally contacted the NY health department to corroborate some
claims I found on the Igenex site that cited the NYHD as basically
endorsing the lab. ( I may still have the e-mail exchange and could
try to locate it if you are interested)

As for babesia testing I guess the most reliable thing is blood smear
at a reliable lab. If they see the distinctive double rings is
probably most definitive. I don't mean the Fry labs though. Any
standard commercial lab. As for the other babesia testing at Igenex
and MdLabs or bowen labs, well I wouldn't bet the house on their
reliablity myself.

I did blood smears myself (Giemsa stained) ( like I said I come from a
scientific background and was able to ask some friends to help me
out). It wasn't clear that it was babesia, I asked different
scientists (in pathology and hematology) but it was clear my blood
didn't look right, (as a matter of fact it look more like malaria than
babesia, but I couldn't be exposed to malaria, well very unlikely)

Well I guess to be clear, if on smear you see the distinctive double
rings, great. If not it doesn't rule it out.

It was not clear, there was always the doubt it could be an artifact
(for me) .However, even a Ph.D pathologist that I asked help for
pointed out that it indeed look like malaria infection and that is was
not an artifact


Babesia by the way is in many ways similar to malaria and infects and
affects red blood cells, it is an erythrocytic infection. In a smear
you might or might not see an rbc that is perfect to view the classic
sign the double rings but not every rbc is gonna show that. Depends on
how many rbcs are infected, the stage of infection, which rbcs you
happen to see in the smear and your view of them etc.

yes unfortunately I saw the rings but not the maltese form

And without knowing some travel history I couldn't say whether it is
likely or unlikey that you have malaria vs babesia. But assuming you
live in and stay in the us and haven't travelled someplace where
malaria is likely, yeah it probably isn't malaria.

I actually do travel to a place where there is malaria, however very
rare





By the way Lyme is known to cause demylienating nerve disease

really?, but a demylienating nerve disease is pretty much attributed
to immune system dysfunction, and any infection could cause this in
any predisposed individual.

Well not every immune system dysfunction causes nerve demylienation
nor autoimmune disease.
sure, I hope I didn't imply that.

I also don't really like the term autoimmune I
believe that what is thought to be autoimmunity in body's immune
system attacking itself is really the immune system attacking low
level infection, so I think it is really hyperimmunity.

I agree in the sense that in some cases a low level infection causes
immune dysfunction (i.e hyperimmunity ) again in predispose
individuals. But in M.S and CIPD for example is clear that that
proteins produced by the immune system attack the myelin sheath in the
CNS and PNS respectively, in fact by electrophoresis you can
distinguish which proteins are attacking what "antigens" in the
myeling sheats of the CNS or PNS, this doesn't exclude that it could
be a result of an over response to a low level infection, but it could
still be present even in the absence of any pathogen.


I basically
don't think the idea of sterile autoimmunity makes much sense. How
could the body's immune system be that dysfunctional and we still
survived?

well many actually died because of that an still due (take for example
CD4+ T-Lymphocytopenia just to mention an obscure one, but simpler yet
allergies), not only that, infectious disease was thought to be dead
in the water but as we have seen there has been an incredible amount
of emerging new infectious diseases. Also think about all the toxins
were are exposed nowadays? have you read about the frightening raise
of allergies and autoimmune disorders incidence in the last 10 years
(in the U,S)? see how many kids in schools need to have special menus
to avoid going on anaphylactic shock. Cancer as well is linked to
immune dysfunction, since is the immune system the principal "agent"
for preventing cancer, in fact putting the immune system in overdrive
is now used in clinical trials (with great results) to combat cancer
such as Melanoma (an acquaintance had it and is in remission now), of
course you could foresee the risk associated with that (the side
affects are also very gruesome but transient, at least in the case I
know). Now relate the incidence of Cancer with the degree of
industrialization in a country. For me it would be actually rare that
a system as complex as the immune disease could evolve fast enough to
protect us from all the new different allergen/pathogens that we are
exposed to.


Problem is that prior to PCR testing we could only find
antibodies. Once antibodies are done and infection is in immune
privileged sites the immune system is still attacking antigen not self
in my theory just now can we detect low levels of antigen that were
undetectable before.

Actually indirect IFA, doesn't require antibody response (the antibody
has been produced previously and comes as part of the assay kit)

If the body's immune system were so dysfunctional
that it kept attacking the self once the antigen was gone how could we
as a species have survived, why wouldn't something that dysfunctional
have been selected out?

same as before, same with cancer ("why wouldn't something that
dysfunctional have been selected out")



What else is a proven demylienating agent? only proteins (antibodies) produced by the immune system (some still say is believe to). In terms of triggers, anything that you can imagine was been hypothesized. Demylienation is not a direct consequence of lyme but of the immune system. In fact rodents with huge loads of lyme do not developed demylienation process however they develop symptoms similar to humans early during infection. M.S rodent models are usually obtained through inoculation of viruses to induce immune dysfunction. These viruses are developed and manipulated on purpose to mimicry the proteins of neurons.



would chose LDN over Colostrum, which I did, maybe I should take both
but if my situation is autoimmune which I believe if it is then LDN
would be a better option (which I'm taking)

LDN???

Sorry, it stands for low dose naltrexone, Penn state university
released a study showing the efficacy in Chron's disease, there was
only anecdotal evidence before on different autoimmune conditions,
specially M.S. Right now, after this study came up, the M.S society
had collected enough funds to start their first trial. Nobody really
know how it works, it is believed that a short transient blockage of
the opiod receptor results in upregulation of endorphins, which are
believed to play a major role in the immune system.


Is your thought that a false negative ELISA is really that common and
not really a tool for at least discarding lyme?

Absolutely. Elisa probably has a 40% false negative rate. Best
evidence besides reading pretty much every paper about testing and
patent applications is the lyme vaccine trials, a large cohort of
patients studied and a 35-40% false negative on ELISA. Which is not
the sensitivity one wants in medical testing. Then there are
specificity issues too. Pretty much a coin flip.

Do you have the reference to that paper? specifically the one about
the lyme vaccine trials?


What is statistically and scientifically crazy and outrageous is that
the current recommendations are that the ELISA be used as essentially
a screening test for the wb which given the restrictive criteria which
include eliminating from considertion specific bands because they
would come up if a patient had the now off the market vaccine (rather
than asking patients did you have the vaccine when interpreting the
significance of those bands ??? which I guess makes too much sense and
the whole thing isn't an issue since the vaccine is gone anyway...)
but the WB turns out to be little better if at all.

So rather than requiring apositive wb to confirm a positive elisa
given the high false negative rate on both tests, might as well just
flip a coin and skip the two step testing altogether.

not really, let's assume that a person with lyme (that was has lyme
antibodies in his blood got tested with an ELISA, let assume as well
that the % of false negative of the Elisa is 50% (an that's even
including the error of those who do not have the antibodies), that
means that chances he gets a false negative are 0.5, just like you
said flipping a coin, but if he were to get another ELISA and his test
came back negative again, it would be the same probability of tossing
a coin twice and getting the same result, which according to
probability is 0.5*0.5 =0.25, 25% now take into account the
probability that you have lyme but as well didn't have a rash say is
50% as well (which I really doubt but let's go with ILADS). Now the
probability that you tested negative in 2 independent ELISAS, that you
didn't have a rash but still have lyme is now : 0.25*0.5 = 0.125,
12.5% now include the probability associated with prevalence of the
disease in the area you live etc....but apparently everyone won the
lottery, at least at lymenet.


taking away those who
don't produced antibodies or those tested before they developed them.

Yes well those are potentially two large groups and if you add those

but that's just speculation

in whom antibodies might not be detectable because of prior or current
treatment and other issues, well the testing sucks totally.

thanks again-

Hey no problem. Let me know what you think of that paper.

good discussion..



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