Why PCR testing, antibody assays and biopsies don't detect intracellular bacteria
All you can detect with PCR testing are those bacteria which are being killed.* It is not possible to identify the species which are most successful, because they are not being killed by the immune system, so there are no antibodies, very few RNA fragments, and so they are not detectable. The bacteria are so nicely nestled inside the monocytes/macrophages that PCR will not be able to detect their presence unless the cell membrane is disrupted in some way. After disruption it is likely that the cyto-skeletons will no longer protect the CWD and their RNA may be fragmented/mutated/destroyed by the lysosomal contents. PCR typically looks for small, characteristic, fragments of the 16S RNA.
*Clarification: Bacteria living within the monocytes and macrophages can't be detected. When the cells die (apoptosis or phagocytosis), or when the bacteria leave the cells, it might be possible to see them at that point with PCR, which is sensitive enough these days to detect just a few organisms. Of course - a problem is that you have to be using a PCR probe sequence which is general enough to find the exotic species of biofilm-dwelling bacteria which have been reported ..Trevor..
The antibodies you can find in the blood are the pathogens which have been unsuccessful - the ones that are killed by the immune system. The pathogens which cause sarcoidosis, and indeed (IMO) all Th1 disease, do not appear in antibody assays.
Biopsy testing doesn't usually work because the bacteria are destroyed when you take them out of the body; their homeostasis is destroyed and the cytokines in the immune system kill them.
This is fundamental to understanding these diseases - they are due to "Stealth Pathogens". The Th1 parasites have very comfortable homes and are no longer being recognized as pathogenic by the host immune system.
They are the truly successful pathogens and they are the cause of Th1 disease. The reason the autoimmune diseases are still idiopathic (unknown cause) is that folks keep looking at what they can easily see, instead of putting all the clues together to infer that there must be somethig else, and then go look for that 'something else'.
The MP was designed to be effective against 'something else'.
CWD bacteria only move out of the infected cells when the cells die. They use biochemical mechanisms to delay apoptosis, and make the cell stay intact as long as possible. When in the bloodstream the pathogens are protected by the biofilms that you see in the videos I have been showing.
..Trevor..
Mar08
Back in 1978 I wrote a paper "Electronic Design Educating for an Uncertain Future" where I was wrote about "tackling .. tasks where the starting data may be vague, or incomplete, and where many alternative solutions may be equally valid."
The Idiopathic diseases present us with a very similar set of disparate and incomplete data. We can detect parasitic genomes, in-vitro, but have little data about whether they are active in-vivo, or what their effects might be, in-vivo. Additionally, there are tantalizing hints that other parasitic entities might be present, even though we can't detect them.
The Wirostko TEM micrographs, for example, showed a microbiota totally unknown to Medicine, yet clearly present in the patients Emil and his group were studying. Similarly, there had been many, many studies linking various known pathogens to Sarcoidosis, and CFS, yet none of them were clearly causal, as none of them were present in every individual.
The CFS patients in Australia, for example, who, if seropositive, were usually so for Rickettsia, suffer identically to those in the USA, who are often seropositive for Borrelia. Clearly neither of these pathogens were causal, and there were factors in play which were unknown, interacting in ways which were poorly understood.
That is why I took a different approach back in 1999. Building on my experience dealing with uncertain data and outcomes, I decided that in-vitro testing, the Gold-Standard of Medicine, just had to be missing something important. Similarly, the animal models were not producing results which were portable to human experience, so they, too, had to be set aside.
Thus, having discarded a century of studies, a century of what was thought to be "knowledge," I started to re-examine chronic disease based on the tools and techniques which had been developed for modern genetic biology. Trying to piece together the clues from a tiny subset of available perceptions and data, into a model which would be rigorous, and which would exactly describe the human experience. By its very nature, this study dealt largely with the philosophical. Only in later years did the science fall together into the rigorous mechanistic model we now have elucidated.
It is meaningless to focus on a virus, fungus, or bacterium which can be easily observed. Otherwise the pathogenesis of chronic disease would have been described decades ago. Being able to culture pathogen, or detect it with PCR, gives no clue as to whether that pathogen is causal in the disease process, or just present as a result of the immune system being weakened by an underlying disease process.
I know how tempting it is to apply the lab techniques of yesteryear to the imponderable problems of today. But one needs to start thinking, instead of focusing on observations. The fundamental problem with observational science is that unless you know what you are looking for, you don't know how, or why, to observe it. What is needed in modern medicine is the discipline of Planck and Einstein, the discipline of working with dilemma which defy description, and puzzle out, by sheer philosophical discipline, what the inter-relationships might be, in order that the data can then be experimentally observed, ranked, and the model verified.
..Trevor..
See also What is a therapeutic probe?
Last edited on Mon Mar 24th, 2008 00:54 by Foundation Staff
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