The Marshall Protocol Study Site > PROF. MARSHALL'S PERSPECTIVE > Prof. Marshall's Perspective > Exactly how do Bacteria change to the L-form?
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The Marshall Protocol Study Site > PROF. MARSHALL'S PERSPECTIVE > Prof. Marshall's Perspective > Exactly how do Bacteria change to the L-form? |
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| Moderated by: Dr Trevor Marshall | ||
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Dr Trevor Marshall Research Team 
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(This topic is dedicated to a certain member of Australia's scientific intelligentsia who recently was reported to make the following ill-informed statement to an Australian member: "I am sorry to say that there is no evidence even for cell wall-less bugs elsewhere in the body in chronic fatigue patients. They would have DNA and that is not there in CFS by PCR assays. You will have made your gut flora tetracycline resistant by selection. The bugs can then be spread elsewhere and even E coli is a hazard to you and other people if you do get an infection needing tetracyclines. Especially likely are urinary infections. We just had a young Indian newly wed in the hospital with this and there is a 20% mortality with even simple infections now.") -------------------------- You know, Medicine, and even much of the Biological Sciences, are still living in the proverbial stone-age, while researchers (like myself) use in-silico analysis and sheer deductive reasoning to leap mountains in mankind's knowledge of exactly how bacteria live, how they survive antibiotics, how they survive boiling water, and the vacuum of space, to come back to a vegetative form when placed in an hospitable environment. At the "Understanding Aging" conference, Adam Arkin, of the Lawrence Berkeley Labs (the folk who brought you the human genome) explained the work he is now doing on deciphering Bacterial genomes, especially focusing on how each gene and protein works.  I took a video of his presentation, and it is available for streaming from our website at URL http://curemyth1.org/flash/adam_arkin.html You will need to upgrade to the latest Adobe Flash Player (you need at least 9.0.115, which was released in December 2007). You will also need a fairly fast computer, as the detail in his slides requires a lot more than YouTube can convey... The presentation can alternatively be downloaded (100 megabytes) from http://curemyth1.org/flash/UABBA-session1.mp4 and played locally, if you prefer. It is in H.264 format, if you don't know what that is then it is best not to bother with the download, and stick with the Flash presentation Here is a key slide, one depicting many of the proteins which determine whether a bacterium transitions to the L-form (he calls them 'spores') or not:  Click on the slide for a full-size version, taken from the full-resolution video. Now, let the discussion begin... |
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Russ Member in Phase 3 
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Whenever I hear about how bacteria can survive in all kinds of the harshest conditions it makes them seem invincible. If they can survive antibiotics and all these other things, you'd think they could survive the immune system's anti-microbial peptides too. Is there something more to the MP - other than activating the anti-microbial peptides via the VDR - that allows us to get rid of them once and for all? Are we "tricking" them by pulsing the antibiotics and maybe getting them to "let their guard down"? Or are the anti-microbial peptides just so highly evolved that though bacteria can survive the antibiotics we manufacture in pill form, they can't survive the ones our immune system has evolved to produce? |
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Dr Trevor Marshall Research Team
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The immune system destroys pathogens by a process of phagocytosis, where the macrophages engulf the pathogen and then digest it by breaking its DNA up into fragments. At that point it is no longer a viable organism. The Th1 microbiota has developed a mechanism to avoid phagocytosis, and live inside the same cytoplasm that would normally digest the individual organisms. |
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tickbite Member in Phase 2/3 
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"pole to pole oscillations 5-20 mins" reminds me of my control systems class. I really didn't like that much math. I guess that picture above is just a generalized scenario. I suppose eventually you could isolate key proteins "inputs" and know how they will form L-forms for a given microbiota. I bet right now, just proving their existence is more important. Open the flood gates! |
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Dr Trevor Marshall Research Team
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I think Alan was concentrating on the Control theory as that was the theme of the conference, and he was the first speaker His colleagues have been isolating the individual proteins, as I chatted with them about this last year during the Metagenomics conference. You might like to review these for more detail: http://www.ncbi.nlm.nih.gov/pubmed/18324309 http://www.ncbi.nlm.nih.gov/pubmed/18573177 |
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tickbite Member in Phase 2/3
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I opened up a can of worms for myself. It really is biomolecular control systems They used Matlab to do the 10 distinct cell history plots. Good program. "It has also been suggested that pathogenic bacteria use cross-talk encoded memory to balance the demands of immune avoidance with a sequential, compartment to compartment infection lifecycle" Interesting..... "If cells could use a memory of past conditions to ‘predict’ future conditions, and delay sporulation, an expensive process, if the environment is likely to improve or accelerate sporulation if the starvation period is likely to be long, they might improve their odds for long-term survival." Most impressive..... Indeed, 'memory' would add to the evolutionary game repertoire. They are smarter than I thought. Thanks for the lesson. |
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Dr Trevor Marshall Research Team
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Greg, Well, at least the ones that have survived for millions (+) of years are very smart indeed. It is always possible that other species are no longer around because their repertoire was less effective |
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Ruth Goold Health Professional
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Trevor, Death from virulent strains of flu (Spanish flu, bird flu) is believed to result from the 'cytokine storm' they produce in humans. As we restore immune function are we becoming more susceptible to these pathogens? I remember a report indicating that it was young 'healthy' adults who suffered the highest mortality in the Spanish flu pandemic, Ruth |
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Dr Trevor Marshall Research Team
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Ruth, We are now starting to understand a lot more about the way that viruses work. Most co-opt human genes to perform necessary functions, such as replication, etc. For example, Bird Flu was recently found to require 6 host genes, of which only two were available in human beings: http://www.ncbi.nlm.nih.gov/pubmed/18615016 One of these discoveries is particularly interesting, the HIV virus, which co-opts the VDR and leaves the host without an innate immune system: http://www.ncbi.nlm.nih.gov/pubmed/17556530 Most of what you will read in the clinical literature about epidemics is incorrect. Indeed, discoveries like those above have shaken the specialty of Infectious Diseases to its core. Indeed, Andrew Noymer has made a persuasive case that deaths from the Spanish Flu were primarily a result of co-morbidity with Tuberculosis: http://www.demog.berkeley.edu/~andrew/1918/PDR_1918_flu.pdf So I wouldn't be too concerned about "cytokine storms" being given as cause of death from these epidemics. And I am totally unconcerned that restoring a human being to health might make them more susceptible to viral or bacterial infection. |
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eClaire Member in Phase 2 
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Given the intellectual level of this discussion, I am nearly afraid to ask, "So, there's no point in my boiling my tap water?" My brother had HIV and his doctors had told him to drink boiled tap water, not bottled or straight from the tap. I figured it wouldn't be such a bad idea for me to do the same given the state of my health. Claire |
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tickbite Member in Phase 2/3
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Unless you live in an area where you cannot get clean, fresh drinking water, there's no point. Personally, I go and get filtered water from the Culligan filling station in Walmart. Otherwise, I think the reference to HIV up top suggests that the MP may be one day the cornerstone to recovery from AIDS/HIV. Gotta have a functioning VDR. In other words, you have to have a functioning innate immune system just as those who are doing the MP. Microbes are everywhere, it's part of the natural world. |
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Freddie Ash Member in Phase 3 
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HI ALL This is Fred in WV. I think, if I understand the MP correct, that when our immune system is working, we should not be catching any or very little bugs that our own immune system will not kill before the bugs can get a hold on us and make us sick. Remember, we are all in this together and I am pulling for us. Your friend in Sarcoidosis Freddie |
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eClaire Member in Phase 2
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Well, I can filter the water through my refrigerator system or through the tap, and so I guess I will move to that system of extra filtration (used to have one on the tap in the old house and when I bought a new system it wouldn't fit with my new faucet and I was never well enough to get the problem straightened out...think I could manage it now). Well, of course, given what we know about the MP, it makes sense that people who have had an STD and strong antibiotics and have taken steroids are more likely to "catch" HIV and develop AIDS, then those who haven't. My brother never took "steroids," but he did get an STD that was antibiotic resistant (supposedly) and took abx for it, and he was seriously addicted to whole milk from a young age (hmmm...let me see if there is a seco-steroid connection there). I wish he had just held on a few more years; he could have started the MP with me. As it was, I was following in his footsteps with Th1 illness of my own (diagnosed as CFS) and believe that before starting the MP I probably had about 6 months to 2 years to live. Given all of my heart IPR since starting the MP (my brother died of congestive heart failure and an infection that overtook his lungs), I believe the MP saved my life in the last year. Claire Last edited on Sun Jul 13th, 2008 00:19 by eClaire |
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Dr Trevor Marshall Research Team
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eClaire wrote: Well, of course, given what we know about the MP, it makes sense that people who have had an STD and strong antibiotics and have taken steroids are more likely to "catch" HIV and develop AIDS, then those who haven't. No Claire, that is totally wrong. Our data shows that after the MP, and while folk are in Phases 2/3 of the MP, they are far less likely to succumb to any bacterial or viral disease (or indeed, cancer) than the general population. It is not possible to draw any generalizations for folk who are not on the MP, although if they are stil on steroids that does place them at higher risk of recurrent or new infection. In this category I include those who are taking Vitamin D supplements. As for using filters - forget it - there are no filters small enough to catch the L-forms which are making you ill  Last edited on Sun Jul 13th, 2008 00:52 by Dr Trevor Marshall |
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eClaire Member in Phase 2
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Thanks for correctly that as totally wrong, as I was just repeating what I read about HIV/AIDS risk factors. Thanks also for clarifying the need to a filter. If I put one in, it will be about the taste of the water. Claire |
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garyv Member in Phase 3 
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If you MP pros will indulge a newbie, I would like to offer the opinion that, even with a disabled VDR, the human immune function can still deal fairly effectively with the standard (non-CWD) bacteria/viruses responsible for seasonal flus and colds. I say this because 20 years ago, at the age of 35, I began to suffer bouts of severe fatigue/low energy paired with abdominal cramping, bloating and general discomfort. I also continued to experience, as I had for my entire life, sinus infections at least twice/year with congestion/drainage lasting about 2 weeks/episode, often moving to throat and bronchial passages before ending. As I began shifting my diet, first to unprocessed foods and then to Paleolithic-style (no grains/dairy) eating, my abdominal symptoms and seasonal infections gradually abated. I can now say I have had no colds or flus or digestive problems whatsoever for the past 6 years while my energy level made a corresponding increase to that which I enjoyed in my 20’s. HOWEVER, what I have recently recognized, after encountering Dr. Marshall’s work, as my Th1 issues, which include osteoporosis, Raynaud’s, paresthesia, leg/foot cramps and tinnitus, continued on through the dietary changes undiminished. In the past year I also experienced a re-emergence of osteoarthritis (hips), which I previously experienced 10 years ago but put to rest at that time by quitting white potatoes (the final change I made in moving to a 100% Paleo diet). Since my mother and grandmother and only sibling (sister) also have a plethora of Th1 symptoms, I believe I’ve been CWD-infected for my entire life. But, it seems to have been my metabolically inappropriate eating that pushed me over into susceptibility to 100+ infections of the standard sort over the years. And, of course, the antibiotics I was given for those no doubt exacerbated my original CWD infection and enabled it to manifest sooner than it might have otherwise. My arthritis experience seems to indicate that certain Th1 symptoms can be mitigated, or at least postponed for a time, by a metabolically appropriate diet, but eventually, as the CWD bacteria proliferate and the VDR becomes evermore disabled, Th1 disease comes to the fore in various ways, as determined by lifestyle and genetic inheritance. Does this “thesis” make sense? Has anyone else out there in MP-land experimented with a Paleo diet? Curiously, garyv (5 months into Phase 1) |
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Dr Trevor Marshall Research Team
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GaryV, You are incorrect. Your GI tract problems are due to the Th1 pathogens, indeed, they probably started to populate your body tissues from the gut. The Th1 pathogens cause a cytokine release which unbalances the other parts of the immune system. For example, giving rise to the antibodies which have been called "autoimmune." Your diet may have helped with the GI symptoms, and even with the rate of spread of the pathogens, but ultimately the microbiota will win, no matter what you eat. These bugs have been around Homo sapiens at least since the Neolithic period. With a disabled VDR the human immune system cannot function, nor can its cancer defenses. Full stop. There is no doubt... |
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garyv Member in Phase 3
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Thank you, Dr. Marshall, for your most helpful reply. I can certainly see where the CWD pathogens could be the responsible agents for my gut issues, which I may indeed have only put into a temporary "remission" of sorts with my dietary restrictions. It still seems, however, that the increase in vitality and apparent immunity from colds and flus that I also experienced might be due to an unburdening, if you will, of my immune system from having to deal with antigenic breakdown products of metabolically inappropriate foods. It's also occurred to me that such dietary restrictions may be helpful in mitigating immunopathology as I proceed through the MP. I guess time will tell! A final thought: It's most interesting that you mentioned Neolithic times as the period of genesis of the CWD pathogens, since that is also the period when man began eating grains and dairy products that had never before been available to him. Might this confluence signify some form of symbiotic relationship? With gratitude, Gary in Virgina |
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dymi Member in Phase 3 
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I would like to ask maybe stupid question. But could someone tell me what are the little moving dots on the life blood analysis (visible only in dark field). Naessens calls them somatides. They seem to be in every life blood picture including Andys Write's famous video. I would like to know the MP point of view. for example this video: http://nz.youtube.com/watch?v=Py-hutc5ZNM Thx. Petr Last edited on Wed Jul 16th, 2008 20:42 by dymi |
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Dr Trevor Marshall Research Team
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Petr, These artifacts are not what are making you ill. Anybody can set themself up as an expert on YouTube. But nobody else has dared to encourage their "successes" and "failures" to freely communicate over the Internet. Focus on results, not on personalities or vague promises. |
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dymi Member in Phase 3
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Yes Dr. Marshall, but they seem to be too "lively" to be part of brownian motion. The polymorphism (as the rod forms a round body and then it divides in three parts) in the end of the video looks kind of astonishing to me. Do you think its a fake? Last edited on Wed Jul 16th, 2008 21:49 by dymi |
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Dr Trevor Marshall Research Team
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Stop focusing on the wrong things. This is what has distracted Medicine from the real answer for a Century. I said that these artifacts are not what are making you ill. That statement is based on understanding the Molecular Biology behind disease. Start thinking about the Molecular Science, not looking at things where you can't even begin to understand the conceptual complexity. The key is how the pathogens evade the innate immune system. This researcher does not even begin to contemplate that issue. |
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dymi Member in Phase 3
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You know, I am an aeronautic engineer. I like to watch thigs that move and analyse why :o) I see that there are litle tiny particles that seem to organize themselves in the blood plasma, I have difficulties to get convinced that they are just fragments or some debris from cell apoptosis. I have seen the long biofilms in the Andy Wrigt video and it seems they contain also these at some locations. In fact if you look closer, the particles seem to have a little flagella that propels them. You really don't think that that are some kind of bacterial speacies (mycoplasma etc.)? Did somebody study these under the electron microscope? (probably difficult task). And your opinion on R.Rife? To me it very corelates with your research. Just people call it differenet names. |
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Dr Trevor Marshall Research Team
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I never said that these artifacts were not bacteria, fungi, or other pathogens. I said that these were not what is making you ill. It is the Molecular Biology which tells us that. Please be careful that you read precisely what I am saying. As for electron microscopy, please look carefully at my presentation at UCLA a couple of weeks ago: http://www.vimeo.com/1270611 And please read our FAQ on Co-infections. ps: Rife technology does not destroy the intraphagocytic metagenomic microbiota which causes Th1 disease. Last edited on Thu Jul 17th, 2008 14:43 by Dr Trevor Marshall |
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dymi Member in Phase 3
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I know thanks to MP that Emil Wirostko made wonderfull images of the CWD inside the white blood cells. I ment if you heard about somebody who tried to study at higher resolutions the singe particles (or whatewer it is) that are moving freely in the plasma visibly under dark field. They must have something around 200-300nm if the red blood cell has 7.5 microns. Your presentation is impressive.... To the prostatic hip joint and heat vent bacteria. :o) I would think that some of the bacteria get there as the contamination of the implant. Maybe it would not be present in person without implant. Last edited on Thu Jul 17th, 2008 14:50 by dymi |
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Dr Trevor Marshall Research Team
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Contamination? ROFLMAO Let's have no more of this nonsense Dymi, my patience is exhausted. |
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dymi Member in Phase 3
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I did not mean it the way it was formulated. English is tricky for not native speaker. I just wanted to point out that if the person did not have the METAL implant, maybe this type of bacteria would not have the neccecary conditions for their survival. http://www.divediscover.whoi.edu/hottopics/bacteria.html "Many thermophiles have a simple diet, based solely on the metals, gases and minerals that comprise the hydrothermal vent fluid. For example, on Knorr we are growing thermophiles collected from vent sites in the Indian Ocean that require only sulfur, hydrogen and carbon dioxide." I agree contamination is not the correct term, and I did not inted to upset you. Best, Petr |
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MarkN Member in Phase 3 
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Petr, The bacteria that have adapted to live in hot springs (thermophiles) are completely different from the bugs that are making us sick. They probably couldn't even survive inside our bodies. The study on the prosthetic hip joint really does show us what kind of bugs are living inside the body. |
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dymi Member in Phase 3
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I will have to read the full article that Dr. Marshall refferences. In his video of the presentation there is among the others: hydrothermal vent eubacterium look at: http://www.palaeos.com/Kingdoms/Prokaryotes/Thermotogales.htm http://www.palaeos.com/Kingdoms/Prokaryotes/Eubacteria.htm Eubacterium is a large bacterial family but the hydrothermal is rather small subgroup of bacteria that lives in the hot water. It uses some metals for its metabolism, sulphur etc... My point was only to question if the fact that we add a foreign metallic object to the human body could not make the human environment more suitable for some atypical bacterial species. What would be interesting to explore is the original damaged joint (that was replaced by the implant), make DNA research there, and then after 10-15 years of service to repeat on the degraded implant of the same patient. Kind of diffcult long term follow up study (doctors don't have patience to do things like this ...too much egineering approach;-). Last edited on Mon Jul 21st, 2008 14:25 by dymi |
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Dr Trevor Marshall Research Team
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OK Dymi, enough, already. Your point about the presence of metal was quite clear the first time you made it, and you are trying my patience with this repetition. As it says in your citation "The Thermotogales make their living by scavenging biomolecules, including amino acids, glucose, sucrose, starch, cellulose, and xylan." Please do not try to ponder the science until you get to to the stage in your recovery where you can do it without fixating on this or the other individual concept. Your idea is a good one, but is nowhere near the complete picture. Meanwhile It has little to do with the topic, which is "How do bacteria change to the L-form" Please do not reply to this. I want to get this thread back onto topic. Here we are talking about a metagenomic microbiota, and how bacteria change to and from the L-form (in that microbiota) and the more studied walled forms. Last edited on Mon Jul 21st, 2008 15:24 by Dr Trevor Marshall |
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NorCalJim Member in Phase 3 
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I understand that the microbiota have been observed by a few researchers inside the cells and as the escaping biofilm tubules. Is there any possibility to do a before and after the MP series of photos or videos of them? Thanks, NorCalJim |
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Dr Trevor Marshall Research Team
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NorCalJim, None of our cohort had "before" images taken, and those patients who supplied the blood to Dr Andy Wright have not recovered, they have not been on the MP. The bigger problem is that this microbiota exists in healthy people, too. Inter alia, it determines the diseases of aging. Everybody has them, only the metagenome differs (the species present). So there really is no 'control'. One of our members microscoped the blood of the members of his son's soccer team. He found the microbiota in all but one of the kids. Does that help you understand the magnitude of the conceptual difficulty if one were to use the presence of this microbiota as evidence of disease? Everybody has them, it is just that Medicine hasn't really noticed them before... |
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Rico Moderator
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It's incredible that medicine hasn't yet noticed the intracellular pathogens. Trevor, is it the volume of microbiota that end up making people sick in the end? Sounds like Vitamin D didn't come first, then (chicken and the egg) - Vitamin D is one of the factors contributing to an increase in chronic illness but sounds like the pathogens will do us in eventually anyway since we all have them. |
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Dr Trevor Marshall Research Team
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Both the volume and the specific genes affected by the microbiota contribute to disease and aging. History shows that the pathogens will 'do us in' anyway. The key issue is that eradication of the key infectious diseases with the advent of antibiotics in the mid 20th century ought to have increased longevity more than it did. Both the overuse of beta-lactams and Vitamin D contribute to this. Possibly also a sun-loving lifestyle (bikinis, big windows, convertibles) |
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jrfoutin Research Team 
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A speculative "why do all roads lead to Rome?" evolution advantage question for bacteria that change to the L-form, rather than a "how is it done?" question: Has the pathogen/L-form change sequence evolved enough to have a distinct advantage in host death (dominant species or subspecies or community life cycle changes have an evolutionary advantage)? Or would host death be just an unfortunate currently adverse relic during the community of pathogens (pea soup) or dominant species bacteria to L-form life cycles? I will understand if "why" is is too far off topic from "how". Thank you, always. |
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Dr Trevor Marshall Research Team
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Let's see. Let me answer this in allegory. The species Bacillus anthracis (anthrax) is found in dry soil just about everywhere. It is, of course, in its L-form. It becomes harmful if enough of it collects in the lungs to turn into an acute pathogen. Clearly any L-form which can live in dry soil has an evolutionary advantage over us human beenz And most of them can |
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Veronika Member in Phase 3 
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Dr. Marshall, Is the genetic information (DNA, RNA) of the L-form completely identical to the one of cell walled form of the same species? Or are there some differences? How can the size of the L-form so much differ? (10x-100x smaller) Can we even call it same species? Thx. |
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Veronika Member in Phase 3
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Dr Trevor Marshall wrote: Let's see. Let me answer this in allegory. The species Bacillus anthracis (anthrax) is found in dry soil just about everywhere. It is, of course, in its L-form. It becomes harmful if enough of it collects in the lungs to turn into an acute pathogen. One Q more: Does it mean that the so called "spores" (Anthrax, Mycobacterium) are in fact L-form of the bacteria??? V. |
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Dr Trevor Marshall Research Team
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Sporulation (spores) is the term Adam Arkin gave in the video that headed this thread, and yes, it is another name for the L-form, CWD, Pleomorphic, states of bacteria. In pleomorphs, the expression of genes in the genome into proteins will change depending on available nutrition, harshness of environment, etc. Last edited on Tue Jul 22nd, 2008 16:38 by Dr Trevor Marshall |
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Markt9452 Member in Phase 3
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The species Bacillus anthracis (anthrax) is found in dry soil just about everywhere.
"The binding of infectious agents in soil actually greatly enhances the infection," Aiken says. "It makes the disease more transmissible." http://www.sciencenews.org/view/generic/id/8743/title/Persistent_Prions_Soilbound_agents_are_more_potent |
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Dr Trevor Marshall Research Team
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Well, yes, except please remember that at Karolinska we we told (effectively) that prions are probably not the infectious agents, and that the Th1 metagenomic microbiota are the agents which are infectious |
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Frans Member in Phase 2 
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Trevor, when looking through the schedule on page 2 of http://www.ncbi.nlm.nih.gov/pubmed/18324309 under the schedule they state that they have omitted an ellipse with Biofilm formation... which is of interest for us I think Secondly, unfortunately, I cannot follow mr Arkin in detail in his presentation, so I am not entirely sure what exactly happens during sporulation. I don't hear him saying that they shed their cell walls, but somehow layer it with proteins? Another thing (I think) he says is that the bacteria dehydrate ? What would that mean for their size ? I would think this explains why they get so extremely small ? Did mr Arkin say how small they actually get ? This review on sporulation (PMID 16907804) might be of interest for Ames. They actually allowed the bacteria to form Biofilms, since they theorize that competition for food within biofilms will actually lead to sporulation of members of the commmunity. I have been looking for an in detail review of what exactly happens during sporulation, but haven't found one yet. Anyone else find something like it? Best, Frans |
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Frans Member in Phase 2
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bumpy ? |
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inge Health Professional 
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Sorry if this is posted at the wrong place, and I know that few hours of reading on the site could probably have provided me an answer, but here goes: Some 300 ME sick patients, me included, have filed a lawsuit against the state of Norway because of a possible connection with a vaccine project we took part in some 16 years ago. Now that I now that the most likely connection is bacteria contaminated vaccines, how easy would it be to find bacteria DNA or viable bacteria in these vaccines? (They may still have samples of the vaccine left). I know that although one could find bacterial DNA this would perhaps not help our case anyhow, because they would not understand the significance of this. Inge |
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Dr Trevor Marshall Research Team
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because they would not understand the significance of this I don't think I understand the significance of vaccines at this point. The ones using live microbes, like BCG, are clearly going to contribute to the pathogenic load, but it is not possible to generalize about the effect of the others on the immune system. If I had to make an educated hypothesis, it would be along the lines that if you give 'killed' vaccines to people who are already sick it is likely to place a heavy load upon their immune system, and potentially make them sicker. However, the real problem is the increasing percentage of the population who have heavily compromised immune systems so early in life. IMO, Cod liver oil is a factor in Norway, and there are probably others which only a detailed study could properly elucidate. IMO, only after looking at all the factors, could blame be properly apportioned. |
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Claudia Member in Phase 3 
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Frans, I don't know about the heavy science, molecular biology type papers, if that's what you want to read, but if you or anyone wants clear illustrations and plain english, try reading "Sex and the Origins of Death" by William R Clark (1996, Oxford University Press) for a very good explanation of sporulation and a whole lot more about cell biology. I found it to be the best book on the subject for myself, as a layperson, as it had so much info that "clicked" with what I was trying to understand about the MP. Don't be put off by the title - it is a reference to the persistence/immortality of asexually reproducing organisms (like bacteria). This is what we gave up to gain the advantages of sexual reproduction. A must-read.  ClaudiaLast edited on Tue Aug 5th, 2008 17:58 by Claudia |
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Tll6 Member in Phase 3
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Do we not have to make a distinction between spores (endospores) and L-forms. According to one of my text books on bacteriology endospores are formed by only 2 genera of bacteria both of which are gram positive: the aerobic Bacillus and the anaerobic Clostridium. Endospores (as in the anthrax spores) have a layered protective coat consisting of: a cell membrane, a thick peptidoglycan mesh, another cell membrane, a wall of keratin-like protein, and an outer layer called the exosporium. Does that not makes spores very different from L-forms. |
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Dr Trevor Marshall Research Team
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W. Ford Doolittle argues cogently against the concept of species at this URL: http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/doolittle.rm Anthrax spores are commonly referred to as L-forms. I think that it is likely any text which divides the phylogroup up so tightly into just a couple of species is bound to be overlooking the big picture. On the other hand, studies that only look at genera, such as the human skin study http://genome.cshlp.org/cgi/content/abstract/18/7/1043 tend to leave the feeling in this reader that they were not precise enough, even though that feeling is totally without basis In our case, the focus is on the microbiota itself, and the power of its metagenome. That environment tends to make me a little less concerned about physical attributes than I am about individual genes in the metagenome, and how those genes map to to the human genome, with the potential for interference with the mechanisms by which the human genome repairs and replicates itself. |
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Tll6 Member in Phase 3
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I will defer discussion for the time being about what is or isn't a L-form because: Has anyone connected with the MP looked at or read the National Academy Press document "Size Limits of Very Small Microorganisms. Proceedings of a Workshop". This document is a mind blower. This document could be required reading for anyone who wishes to explore what might be the nature of Dr. Marshall's "pea soup" of intracellular organisms. It considers many things from sizes of various components of cells, RNA, DNA, ribosomes, cell membranes, osmotic pressure, nr of proteins, metabolism, biophysical constraints, nrs of genes, genome size, free living organisms, non free living organisms, and many other subjects. There is even a postulate of a kind of living in consortia rather like Dr. Marshall's "pea soup". |
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geirf Health Professional
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According to Andrew Wakefield there have not been made any long term studies on safety of MMR vaccines. According to prof Tore Midtvedt , Karolinska Institute Stockholm, when MMR (three live viruses) was to be introduced to Sweden , they opposed to use the vaccine, as they were sure the vaccine was not safe, and could be containing Mycoplasmas and / or Chlamydias. During a foreign trip of the head of Karolinska the MMR vaccine was introduced, he cried when he came back and got to hear they were now using the MMR vaccine. Vaccine Measles virus is a good candidate to explain Autism, but of course , also here the virus might well only be a coinfectant , or of course be a co cause together with a L-bacteria. ? |
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Dr Trevor Marshall Research Team
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Gier, As I have already said in another topic, Autism Spectrum Disorders result from the same metagenomic microbiota as all the other chronic diagnoses. Forget about viruses - their genomes are not big enough to cause the widespread havoc evident in these diseases. They are just co-infections. The metagenomic microbiota is the root cause, and I now know how it evades the innate immune system, and therefore how to beat it. Take a look at those videos of my presentations I keep pointing you towards... Especially the Keynote I gave in China two weeks ago... |
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vwmusum Member 
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Hi Dr. Marshall - In one of our conversations, I recall you saying something to the effect of, "the overemphasized focus on just tics as the sole, root cause for Lyme is foolish." I hope I am paraphrasing you correctly. I have been unable to get your powerful comments out of my mind on many levels. I have long suspected Lyme is much bigger than the simplistic focus on just tics. We now know there are MANY more animal vectors (chipmunks, lizards, etc.) from the work of Dr. Kerry Clark, et. al. I believe (as does renowned epidemiologist, Dr. Tom Kollars at Georgia Southern University whom I have spoken to and has intense interest in researching here in the US) there are indeed many other insect vectors also. I recall a recent study out of Europe that showed 4% of the mosquitoes were carrying Bb. However, though I am VERY interested in understanding the FULL scope of the vectors carrying Bb and other related pathogens, my question is deeper based on the comment you made to me above. What do you believe is the full magnitude of the Bb transmission? We know, once bitten, we are likely to get a full 'soup' of pathogens and mycoplasm in addition to just Bb. However, as I and many others strongly suspect, are there OTHER ways of getting Lyme than just insect bites (congenital, sexual, salivary, transfusion, food supply transmission, etc.)? Moreover, is it possible that virtually EVERYONE to one level or another has some degree of Inter Phagocytic, Metagenomic, Microbiota? I know the implications of this question are staggering, yet science facing the full answer is imperative. If so or not, what is the BEST BLOOD TEST to see if someone is in need of the MP? Is it just a test of the Vitamin D and the 1, 25 D levels as Dr. Fein did (along w/a whole other battery of tests) on me and also mentioned in Bryan Rosner’s book, The Top Ten Lyme Disease Treatments? Finally, when we spoke of CWD forms and Mattman's groundbreaking book on them you made a comment I do not even wish to try to paraphrase, but I sensed it was very important. What is the latest understanding of her work and the CWD forms for the lay person? I take it the CWD forms, while critical, are far from the whole current story on chronic illness. What are there differences for the lay person between Inter Phagocytic, Metagenomic, Microbiota and CWD L-forms, mycoplasm and other rarely understood In-Vivo bacteria? FYI, when I met last year one on one w/Dr. John Halperin on the board of the IDSA at his hospital - Overlook, Summit, NJ - we had a rather lengthy and pointed "discussion" on the awful positions he and his colleagues had taken for us patients. Among several instances where a lay person like me had him utterly outflanked, he was completely UNAWARE OF MATTMAN's work. He wanted to borrow my copy of her textbook! I was astounded that someone making critical medical policy at the highest levels of this county had not even read a book referenced in virtually every other book I have read on the subject of Lyme disease. |
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edj2001 Moderator 
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I just completed a Cell Culture Biotechnology class and became aware of the problems associated with cell culture contamination especially by Mycoplasma. Of course this is in-vitro but it is interesting to see how the bacteria are able to infect the cells. Take a look at the following report. There are specific references to Mycoplasma contamination. Ryan J PhD., “Understanding and Managing Cell Culture Contamination”, Corning Incorporated Life sciences http://catalog2.corning.com/Lifesciences/media/pdf/cccontamination.pdf |
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Shari Gold Member in Phase 3
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Hi Dr. Marshall.... Just curious about this article that I just found on my web browser. Have you read any of this in any of your recent research .. and what do you think about the team using "ferrets" for the in vivo portion of the experiment???? Best, Shari Gold Full article: http://news.aol.com/health/article/researchers-solve-1918-flu-mystery/289681 Re:... solving the riddle of the 1918 flu pandemic (excerpt from Yahoo browser story) "We wanted to know why the 1918 flu caused severe pneumonia," Kawaoka said in a statement. They painstakingly substituted single genes from the 1918 virus into modern flu viruses and, one after another, they acted like garden-variety flu, infecting only the upper respiratory tract. But a complex of three genes helped to make the virus live and reproduce deep in the lungs. The three genes -- called PA, PB1, and PB2 -- along with a 1918 version of the nucleoprotein or NP gene, made modern seasonal flu kill ferrets in much the same way as the original 1918 flu, Kawaoka's team found. Most flu experts agree that a pandemic of influenza will almost certainly strike again. No one knows when or what strain it will be but one big suspect now is the H5N1 avian influenza virus. |
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Dr Trevor Marshall Research Team
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Shari, I have no idea whether ferrets are a good analog of man's immune system, nor whether the isolated flu genes behave the same way when transfected as they did in the native flu organism. Studies like this are of little value until they lead to tangible results. I had a series of discussions with Nobel Laureate Peter Doherty about a year ago. He has spent the last decade trying to find a vaccine for the HIV virus. He made it clear to me that the behavior of a virus, which is an organism which derives most of its genes from its host, is extremely complex, and extremely variable. Based on those discussions, I feel that this ferret research seems a bit simplistic, but I may be wrong. You will find previous discussion here about the 1918 Flu, there has been a persuasive hypothesis advanced that TB was involved as well as a virus. |
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vwmusum Member
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Hi Dr. Marshall, I was following up on my Dec. 27th post. One essential part of my post asks: "What are there differences for the lay person between Inter Phagocytic, Metagenomic, Microbiota and CWD L-forms, mycoplasm and other rarely understood In-Vivo bacteria?" It would be very helpful to gain your understanding of what seems to the lay person (much less medical professionals and microbiologists) a confusing list of all these often referred to bacterial forms. This would include those listed above in addition to the “Bio Films” Dr. Alan Macdonald has pioneered the discovery of and any other important forms you feel need to be defined and understood by all. Is all the micro-bio nomenclature describing essentially the same thing? That seems unlikely again to the lay person. It would be VERY helpful to gain a deeper understanding of this. I believe that would allow us all much better insight into what we with chronic illness are up against and what the MP is so successful at overcoming. Despite reading extensively on the subject, I would most gratefully defer to you. Based on my conversations with numerous medical professionals, I believe this understanding; especially from someone of your knowledge and ability to bring clarity to any subject would be vital in moving the discussion and wider understanding forward. Would it be possible to list ALL these major various, rarely understood, or widely recognized forms and provide a short definition of each class or group? We are all indebted to you Dr. Marshall and thank you very much. |
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Dr Trevor Marshall Research Team
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What you are seeing is an incremental advance in understanding. Alan McDonald is still looking for species, but microbiologists now realize that species mean very little. The key thing is the way that the genomes interact. See, for example, this video from the Metagenomics 2006 conference: http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/doolittle.rm (W. Ford Doolittle from Dalhousie University (Canada)) Please try and work through my Keynote at the World Gene Congress for the details of why it is the genomes that matter, and not the species: http://www.vimeo.com/2585394 Hence the Metagenomic Microbiota has to be the focus of Science as we move forward, and not the physical shape of the microbial communities. Remember that L-forms were discovered by Emmy Kleinberger-Nobel in 1934. A lot of things have happened since then http://marshallprotocol.com/forum39/6844.html Happy New Year to all... |
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vwmusum Member
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Hi Dr. Marshall, I believe I am starting to grasp the magnitude of the Marshall Protocol. Is it possible almost EVERYONE in one level or another has some degree of Inter Phagocytic, Metagenomic, Microbiota? Should the 2 blood tests for Vit. D and the 1,25 Vit. D metabolite be as common as a cholesterol screening? |
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Dr Trevor Marshall Research Team
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Yes and Yes. |
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vwmusum Member
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WOW!!! I am more motivated than ever to help with your work. |
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vwmusum Member
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Hi Dr. Marshall, I am not sure if you have addressed this somewhere else on the site and I’m not sure how to search it. A close friend of my was a Captain on the NYC Police Force and was at ground zero shortly after 9-11. He has since been diagnosed with 'incurable' sarcoidosis (as many other valiant heroes are stricken with too) who and has been forced to retire on permanent disability. Could the MP work for someone like him? |
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Dr Trevor Marshall Research Team
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Workers at Ground Zero were working under unhygienic conditions, with bodies and body parts, during the cleanup. The best way to look for disease caused by this microbiota is to measure the D metabolites, along with PTH, CRP and other routine bloodwork. |
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vwmusum Member
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Excellent Dr. Marshall. Those were some of my hunches, but there is nothing like getting your authoritative perspective. I will let him know. These brave men and women deserve the best information (which you have) possible to help them. |
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Rico Moderator
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vwmusum, I don't see why your friend diagnosed with Sarcoidosis couldn't be helped with the MP - there have been many other Sarc patients who have: Sarcoidosis Succumbs to Antibiotics - Implications for Autoimmune Disease Antibacterial Therapy Induces Remission in Sarcoidosis Report on a case of systemic sarcoidosis treated according to the Marshall Protocol - by Japanese Neurologist Some Sarcoidosis Success Stories at Bacteriality SARCOIDOSIS |
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jcwat101 Research Professional 
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Trevor mentioned the routine blood work and included PTH (parathyroid hormone). I think PTH is good to measure, but think that it is important to make sure one is getting near the RDA of calcium (in divided dosages) for at least a couple weeks before the test to avoid getting an elevated PTH level due to inadequate calcium intake. And the MP recommendation is that a level of calcium intake near the RDA should generally be maintained after the test. Of course, if you have had problems with hypercalcemia, consult your doctor before taking any calcium. Include the amount you get in food when calculating whether you need a supplement. Avoiding extra phosphate unless you have a known need for it is good (for instance avoid calcium hydroxyapatite supplements or forms from oyster shell that have phosphorus). This is because too much phosphate in people with suboptimal kidney function may also raise PTH. A generally adequate (near RDA) intake of other nutrients that affect bone (eg., near RDA of vitamin K, magnesium, zinc) may be helpful too (should be from food to the extent possible). For more on calcium and when its supplementation may be needed, see: Do I need to take a calcium supplement... Joyce Waterhouse Last edited on Tue Jan 6th, 2009 04:50 by jcwat101 |
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NickBowler Member in Phase 3 
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http://www.newscientist.com/article/mg20126945.400-squid-symbiosis-may-shed-light-on-disease.html It seems that a critical gene for converting to the biofilm form has been researched in squid bacteria (the link to the nature article is embedded in the above New Scientist article). The authors discuss that biofilm formation may have origins in symbiotic relationships between species. |
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jcwat101 Research Professional
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Nick, That's very interesting. Here is something that just came out in Nature- nice to see L-forms getting more attention, especially in a prominent journal. Life without a wall or division machine in Bacillus subtilis p849 L-form cells can derive from various bacterial species and do not possess a cell wall. It is shown that Bacillus subtilis can convert into L-form through a single point mutation, and that B. subtilus L-form cells are able to propagate independent of FtsZ, an essential component of the bacterial cell division machinery. M. Leaver et al. Life without walls : Nature Joyce Waterhouse |
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Martin78 Member in Phase 1 
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The outcome of Cryptococcus neoformans intracellular pathogenesis in human monocytes This study demonstrated that C. neoformans can shed polysaccharide within human monocytes, spread from cell to cell, and be extruded from them. Furthermore, human monocytes responded to ingestion of C. neoformans with cell cycle progression from G1 to S. http://www.biomedcentral.com/1471-2180/9/51 Br Martin |
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Chris Moderator 
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Excellent Dr. Marshall. Those were some of my hunches, but there is nothing like getting your authoritative perspective. I will let him know. These brave men and women deserve the best information (which you have) possible to help them. I just noticed this. If you ever need a first hand story about an MP success, I am available. Chris Raritan, NJ http://bacteriality.com/2008/06/19/interview22/ |
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Frans Member in Phase 2
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Hi all, Heard something on the radio last week and while looking at the latest metagenome presentation, at the point that prof Bushman explains that bacteria might be penetrating the body through the walls of the GI-tract , it struck me that this next paper (which they described on the radio) might be interesting, since it shows another mechanism by which bacteria, in this case E. Coli, can morph into other shapes, even extremely small shapes, so small that filters with micro pores simply won't stop them. I was thinking that if bacteria can move through channels that are only something like half a micrometer wide, where else can they move through? Cell walls? Bacterial growth and motility in sub-micron constrictions. Männik J, Driessen R, Galajda P, Keymer JE, Dekker C. Kavli Institute of Nanoscience, Delft University of Technology, Lorentzweg 1, 2628 CJ, Delft, The Netherlands. In many naturally occurring habitats, bacteria live in micrometer-size confined spaces. Although bacterial growth and motility in such constrictions is of great interest to fields as varied as soil microbiology, water purification, and biomedical research, quantitative studies of the effects of confinement on bacteria have been limited. Here, we establish how Gram-negative Escherichia coli and Gram-positive Bacillus subtilis bacteria can grow, move, and penetrate very narrow constrictions with a size comparable to or even smaller than their diameter. We show that peritrichously flagellated E. coli and B. subtilis are still motile in microfabricated channels where the width of the channel exceeds their diameters only marginally ( approximately 30%). For smaller widths, the motility vanishes but bacteria can still pass through these channels by growth and division. We observe E. coli, but not B. subtilis, to penetrate channels with a width that is smaller than their diameter by a factor of approximately 2. Within these channels, bacteria are considerably squeezed but they still grow and divide. After exiting the channels, E. coli bacteria obtain a variety of anomalous cell shapes. Our results reveal that sub-micron size pores and cavities are unexpectedly prolific bacterial habitats where bacteria exhibit morphological adaptations. PMID: 19706420 [PubMed - as supplied by publisher] Sounds interesting. Frans Last edited on Sat Aug 29th, 2009 00:52 by Frans |
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Phillyguy Member
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Interesting New article on listeria L-forms from Science Daily. September 12, 2009 "For over 100 years, it was known that bacteria may lose their cell wall and can still survive. However, it was believed that this phenomenon was merely an artefact and that bacteria without cell walls do not remain viable. Recent research of a group headed by ETH Zurich Professor Martin J. Loessner, which has just been published in Molecular Microbiology, shows that bacteria without a cell wall can be a stable form of bacterial life. Astonishingly, not only can Listeria survive without a cell wall, they are even able to reproduce and proliferate." "“Culturing” the L-forms of bacteria is not easy. They need to be “bred” in a liquid medium and do not normally form colonies, so plating on a petri dish is not possible. Although L-form Listeria cells are capable of reproducing themselves, this can take time: formation of a visible colony within tubes containing a soft medium takes at least six days, compared to 16 to 20 hours for normal cells." "L-form Listeria can also outwit the immune system. Although macrophages, i.e. phagocytes, ingest the spherules, they seem unable to kill them in a timely fashion. While normal Listeria cells are killed after about 30 minutes, the L-forms can survive for much longer inside a macrophage. The ETH Zurich professor feels that “the immune system may have a problem if macrophages cannot recognise the L-forms as a pathogen.” http://www.sciencedaily.com/releases/2009/09/090912145843.htm Interestingly, listeria may have a preference for the gall bladder and kidneys. I found this interesting since I seem to recall reading that people who suffered acute food poising often develop kidney issues several years later. I believe that it was attributed to structural damage associated with the acute attack, but this never seemed to make sense to me since the issues only appeared years later. Gall bladder issues seem pretty prevalent amongst the TH1 folks as well. http://www.sciencedaily.com/releases/2009/09/090908203427.htm Last edited on Wed Sep 16th, 2009 19:41 by Phillyguy |
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