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Capnine - biofilm bacteria's dirty little secret
 Moderated by: Prof Trevor Marshall Page:  First Page Previous Page  1  2  3  4  5  6  7  Next Page Last Page  
 

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Prof Trevor Marshall
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 Posted: Mon Aug 6th, 2007 12:09

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Dr. Steve Fry at Airpark Medical Center in Scottsdale, Ariz., is hoping the Lateral Flow Assay will help him diagnose his patients' medical problems faster. "This new device will allow doctors to test drugs and materials simultaneously and will save time and money," Fry said.

Well, if it worked as the article advertises it does, then Dr Fry would be finding bacteria in every one of his patients, and trying to puzzle out why. So, based on the above quote, I therefore suspect that this attempt to use antibodies to definitively diagnose disease has failed, as have all attempts before it.
 

tickbite
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 Posted: Mon Aug 6th, 2007 12:13

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I've wondered myself the difference or similarity of biofilm populations on surgical devices and other such "popular" news stories. What is the difference between CWD form biofilms and those such as these?

"The device identifies the presence of biofilm-specific antibodies in patients by allowing the antibodies to bind to biofilm-specific proteins on the device."

I'm also curious about this because i'm under the impression that very few antibodies occur due to successful parasitization of CWD forms, except that early on some pea-soups exhibit some antibody phenomenon ("autoimmune antibodies".)

I wonder what is the "biofilm-specific protein" they are talking about.

~greg



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Prof Trevor Marshall
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 Posted: Mon Aug 6th, 2007 12:45

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Best to ask them, Greg. It doesn't sound to me as though they have any idea what they are doing.
 

tickbite
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 Posted: Mon Aug 6th, 2007 13:51

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:D I've heard that one before.....and they were talking about you! Anyhows, I emailed Dr. Leid. This paper of his is interesting, but still leaves me questioning what connects the dots between big biofilms and tiny coccoid films. I like his description of the contents of the biofilm being "extremely porous hydrogel" :)

weird....



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 Posted: Mon Aug 6th, 2007 20:22

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Greg,

As I understand it, we have both biofilms (which may include CWD and non CWD bacteria) and then we also have CWD throughout the body, independently of biofilms.

That paper you linked to had an interesting quote.  They conclude that:

The mechanisms behind biofilm resistance, especially with regard to leukocytes, are not clear and have been explained by the paradigm of a lack of penetration by the leukocytes and a decreased ability of phagocytes to actively kill the bacteria, a process termed "frustrated phagocytosis"

I suppose we may conclude that capnine or similar VDR blockers are causing the frustrated phagocytosis?

Joyce Waterhouse



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Prof Trevor Marshall
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 Posted: Mon Aug 6th, 2007 20:32

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There are different types of evasion techniques used by intraphagocytic infection. The 'biofilms' photographed by Emil Wirostko's team use one, Mycobacterium leprae and Mycobacterium tuberculosis use a different technique, and yet another is used by the Rickettsias. The subinhibitory dosing of the MP seems to work differentially on Mycobacteria and the 'Biofilm' species. Although ultimately the restored immune system gets them all, we are still trying to gathering data which describes this differential...
 
 

Last edited on Mon Aug 6th, 2007 20:33 by Prof Trevor Marshall

tickbite
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 Posted: Tue Aug 7th, 2007 08:44

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Dr. Marshall,

What does subinhibitory dosing mean?

Well, Dr. Leid came back with a couple of interesting papers.

Intracellular Bacterial Biofilm-Like Pods in Urinary Tract Infections 


Maturation of Intracellular Escherichia coli Communities Requires SurA


He wanted to know a little more about what the heck i was doing. So he may reply again to my explanation and talk more about what he knows. I asked him what he knew of Capnine and the VDR.


It's quite confusing with the HGT cascading mess and the pea-soup conundrum. So many ways to evade the immune system and so many ways to kill the little critters.


~G



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tickbite
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 Posted: Wed Aug 22nd, 2007 11:50

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Bump...

Well Dr. Leid never got back to me :) Interesting papers though. I know someone on the MP who had Interstitial cystitis disappear within the first year.............interesting hugh?



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Prof Trevor Marshall
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 Posted: Wed Aug 22nd, 2007 11:57

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Greg, try this Pubmed search for 'subinhibitory clindamycin':
http://tinyurl.com/27f8wm

you will find a lot about 'subinhibitory' there :)

 

tickbite
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 Posted: Thu Aug 30th, 2007 17:58

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Dr Trevor Marshall wrote: There are different types of evasion techniques used by intraphagocytic infection. The 'biofilms' photographed by Emil Wirostko's team use one, Mycobacterium leprae and Mycobacterium tuberculosis use a different technique, and yet another is used by the Rickettsias. The subinhibitory dosing of the MP seems to work differentially on Mycobacteria and the 'Biofilm' species. Although ultimately the restored immune system gets them all, we are still trying to gathering data which describes this differential...
 
 


Are we essentially saying that biofilm species aren't the only "main" culprits in Th1 disease?

I was under the impression that biofilm species were the main problem, but in light of other intraphagocytic pathogens being successful with other maneuvers, how might the VDR become the king pin otherwise? 

what are the similarities between biofilm species and the others?

~Greg

 

 



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Prof Trevor Marshall
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 Posted: Thu Aug 30th, 2007 18:20

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The species which shut down the VDR, and thus the generation of antimicrobial peptides, are the cause of Th1 immune disease. At this point I do not believe Mycobacteria or Rickettsia persist via that pathway.

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 Posted: Fri Aug 31st, 2007 00:55

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Trevor, not sure if I understand your comment (previous post). Are you saying that at this point you do not believe Rickettsia are directly involved in causing Th1?
And expanding on that question....will the MP get rid of the Rickettsia?


Thanks. Inge.

 

Last edited on Fri Aug 31st, 2007 00:57 by IngeD



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Prof Trevor Marshall
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 Posted: Fri Aug 31st, 2007 09:59

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Inge,
One of the most difficult dilemma I had to resolve, and even more difficult for some patients to come to grips with, is that the infections thought to be causing them to be ill are likely to actually be co-infections, unwitting bystanders at the scene of the crime. These infections are easily observed, but are not necessarily contributing to the illness...

You see, when the innate immune system becomes weakened by the Th1 pathogens which attack the VDR, it can no longer clear viruses, and other infections. Rickettsia and Mycobacteria can be very nasty pathogens indeed, but their mode of action is different from the Th1 pathogens, and they evade the immune system differently. As the body heals, and its anti-microbial peptides start to be produced again, the immune system eventually takes care of fungal, viral and bacterial co-infections.
 

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 Posted: Fri Aug 31st, 2007 10:56

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So is it fair to say that whatever mode of action it is that Rickettsia and Mycobacteria use to avoid the immune system and persist, that mode of action is only effective against a weakened immune system and not a fully-functioning one?



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Prof Trevor Marshall
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 Posted: Fri Aug 31st, 2007 11:43

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Russ,
It is safe to say that these pathogens are more effective against a weakened immune system than a fully functioning immune system.

One paper exploring the mechanisms used by Mycobacteria can be found at
http://tinyurl.com/2wrtpr
with commentary at Nature.com (free access, registration required)
http://www.nature.com/nrmicro/journal/v5/n8/full/nrmicro1728.html
 

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 Posted: Fri Aug 31st, 2007 13:40

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Thank you Trevor. Yes. Hard to accept, but it has been dawning on me gradually since doing the MP and reading up on this site that my illness goes beyond when I thought I succumbed to Rickettsiosis. The whole thing is such a muddle because there appeared to be a point in time when things got really bad. 2002 when I was living in Malaysia and I contracted what the locals called a 90 day chinese cough. Only in my case the 90 days stretched to indefinate.

Now I understand that I already had chronic conditions which go back a lot further than 2002 but which were things I simply had learnt to put up with and put down to all sorts of things! So what must have happened is that I already had Th1 and this made me succumb to the Rickettsia which my immune system was not able to fight off. For 2 years I battled on with steroid inhalors (occasional use) when asthmetic coughs made it hard to breathe. And then I started on antibiotic treatment which did not eliminate the Rickettsia but kept secondary (now understand them to be tertiary???) infections at bay so that I was reasonably comfortable and kept out of emergency rooms. But beneath it all the Th1 was progressing as is evidenced by new chronic diseases becoming apparent (e.g. Peripheral Neuropathy, Hypertension, Insulin Resistance etc) during the last 4 years.

So....the pre-MP antibiotics were killing opportunistic bacteria that my compromised immune system no longer was able to fight off. The MP is killing CWD bacteria and restoring the health of my immune system i.e. fighting the Th1 condition. I then have to hope that this restored immune system will eventually kill the Rickettsia for me to regain full health. Because there doesn't seem to be any other treatment around that can eradicate Rickettsia!

I think my doctor thinks the Rickettsia are to blame for all of my health problems and I had incorrectly assumed Rickettsia to be CWD bacteria. So they are in effect not part of the pea soup? A colleague in Malaysia told me after I was diagnosed with Rickettsiosis: "You sound like a walking biological laboratory".  She obviously knew what she was talking about :( ! So in my case it's pea/ham and whatever soup. Probably some Mycobacteria as well considering the number of times I have had Pneumonia in recent years. Which makes sense considering I have probably had a compromised immune system for many years. Peas soup is hard on the digestion. With the other bits it is giving me a stomach ache :( But...nothing for it but to continue on the fight! There are others here much worse off so together we will beat the buggers! Inge.

 



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 Posted: Fri Aug 31st, 2007 13:51

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Agreed, with the one exception of peripheral neuropathy, which may be due to a secondary infection by Mycobacterium leprae. These are known to be nourished with the epinephrine present at peripheral nerve synapses, where they congregate. So I am not sure about the neuropathy. It might be secondary, and clear up after the Th1 pathogens have been dealt with.

Rickettsia and Mycobacteria are something like the Th1 CWD in that they are obligate intraphagocytic pathogens. But they might not form part of the biofilm-protected intraphagocytic colonies, I just don't know yet.
 

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 Posted: Fri Aug 31st, 2007 13:51

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see Will the Marshall Protocol treat co-infections?



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IngeD
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 Posted: Fri Aug 31st, 2007 15:10

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ok...after one hour of reading (thanks Barb for the link that I seem to understand better now) I am still in a bit of shock re the following:

Dr Trevor Marshall wrote: Agreed, with the one exception of peripheral neuropathy, which may be due to a secondary infection by Mycobacterium leprae. These are known to be nourished with the epinephrine present at peripheral nerve synapses, where they congregate. So I am not sure about the neuropathy. It might be secondary, and clear up after the Th1 pathogens have been dealt with.

Are you say that it is possible to be infected with Mycobacterium leprae without developing full-blown leprosy? I found on the internet that it is now thought that the peripheral neuropathy that people suffering from leprocy experience, and the resulting loss in limbs etc is due to the mycobcactberium leprae. But I did not find a suggestion so far that other forms of peripheral neuropathy are caused by the same bacteria. In 1981 and 1982 we were living in an area where leporsy is still a problem (Northwest Australia). I also read somewhere that it can take up to 20 years incubation for this disease.

Going back to the link Barb provided, couple of comments:

1. I almost want to thank my co-infections because they are what drove me to get medical help. I arrived at the MP missing a gallbladder, 2 ovaries and with a sick liver amongst other things. And had no idea what was the underlying cause.  If it were not for the co-infections being the straw that broke the camels back so to speak, it seems to me that the Th1 disease in its stealthy way could have done a lot more harm to my remaining organs!
2. I also read that fungal infections will be healed by a restored immune system. For years now I had a wart on the palm of my left hand. After 7 months on the MP there is absolutely no trace of it left. Can I then say that my immune system is already more active and that it is the healing immune system that eradicated the wart? Cause for celebration! (the wart may only be a minute issue but if it is a sign that my immune system is already starting to recover..then that is HUGE).

Inge. 



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MP start Jan'07 | Rickettsiosis, gastric ulcers, peripheral neuropathy, chronic bronchitis, adhesions/IBS/Crohn's, pre-diabetes, hypertension | initial 125D=51, 25D=26 | last 25D= 8.4 ng/mL Mar '11 |9.2 ng/ml Feb 12
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 Posted: Fri Aug 31st, 2007 16:07

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Inge,
Truth is, I cannot answer any of your questions about leprosy. Too little is known about it, or why it, and tuberculosis, are currently enjoying a resurgance. In some US states 'latent tuberculosis' may be as high as 10% of the so-called "cured" cases. Is the resurgance due to the Th1 epidemic? Who knows - my recent paper (still in press) did cite a study showing that recovery from Tuberculosis was directly dependent on which VDR gene haplotype a patient has :):)
 
We do have a little data from the SARS epidemic, however. It took out the elderly and infirm, particularly diabetics (a Th1 disease).

I remember clearly one of the diabetic patients I studied in Perth, ca. 1981. He had a foot amputated because it had sepsis. 'Diabetes foot' was the diagnosis, but a young intern from Pakistan differed. He said that he recognized it as "Leper's foot" from his experience in treating the condition in Pakistan. Hmmmm...
 


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