I saw this E. coli 0104 recombination report in Deutsche Welle: Scientists seek answers from origins of 'chimeric' E. coli .. and I thought to myself .. is there something about this shigella toxin producing strain that alters its behaviour inside the stomach or inside the human intestine?
If I was a good micro-biologist I would also want to be a "Remote Viewer" .. or at least have a team of Remote Viewers to consult with. I really don't know why this idea comes into my mind that the deadly combination of E. coli O104:H4 and EAEC 55989 are altering their behaviour inside the human intestine!
I am semi-handicapped here, because I do not totally understand the scientific language; but what I found may hold a tiny clue to the behaviour of bacteria inside and outside the intestines of warm blooded animals and humans.
There is a report from 1961, that may or may not be relevant:
Experimental Genetic Recombination In Vivo Between Escerichia Coli And Salmonella Typhimurium H. Schneider, Samuel B. Formal, and L. S. Baron PDF
I do not know much about the microbiological scientific side; but I do know something about the strange workings of the stomach and large intestine and all its little issues with mold, fungus, yeast and Candida Albicans overgrowth.
I could be wrong .. but perhaps modern medical research spends too much time in mono-hypothisis [I just made that up] .. and this approach leads to a mis-understanding of how things really work in the body.
For example, a micro-biologist may look at cancer cells, fungus, mold, yeast, candida or pathogenic E. coli and bacteria .. but they may not look at how all these micro-organisms interact inside the intestinal environment.
Therefore, E. Coli is E. coli and Candida is Candida .. mold is mold and cancer is cancer. That is what I mean by mono-hypothesis. In the cited 1961 article it states: "In any case, it is felt that the experiments reported here add further to the theory that recombination between organisms plays a role in the natural evolution of the enteric group of microorganisms."
I imagine this is suggesting that enteric microorganisms affect each other and may 'recombine' within the biosphere of the colon (intestines) .. and that we are dealing with a SOUP of organisms who are interrelated and who affect the chemistry of the enteric environment.
For example, all microorganisms have, create and sustain their own chemical environment, in which the bodies immune system has to decide is this beneficial or non-beneficial to the life force of the human, goat, bird, lion and even tree!
The life threatening factor to warm blooded animals and humans could be when a particular microorganism such as E. coli 0104 chemically alters the complete enteric (intestinal) environment. Potentially, altering the acid/alkaline balance and creating multiple complications such as the rapid overgrowth of Candida Albicans (among other things).
Because the 'microbiological detective' is looking for only one cause, they overlook the multiple domino effect of follow on toxins due to a general shift in the intestinal balance. I am thinking that the real devastation may be that the E. coli 0104 pathogen is setting off a much wider chain reaction upsetting many of the intestinal microorganisms (one of which may be Candida Albicans) through chemical changes to the intestinal environment.
The other additional question is why do some people experience more severe symptoms and why do some people experience less severe symptoms? Is it possible that the E. coli strain is altering its behaviour [or severity] depending on the type of microorganisms inhabiting the intestines of the host.
In other words [and I am only guessing], is E. coli 0104 recombining with different strains of intestinal E. coli within the host and in some circumstances recombining with specific varieties of the host E. coli to become more virulent?
Oh! How stupid of me microbiologists already know this! But ... ??
If I was a good micro-biologist I would also want to be a "Remote Viewer" .. or at least have a team of Remote Viewers to consult with. I really don't know why this idea comes into my mind that the deadly combination of E. coli O104:H4 and EAEC 55989 are altering their behaviour inside the human intestine!
Deutsche Welle Report: As of Friday, while German scientists struggled to isolate the source of the E. coli outbreak, epidemiologists and microbiologists remain unsure as to how they can uncover the secrets of this new infectious strain - and ultimately, battle it.
Earlier in the week, a team of German and Chinese scientists said that they had sequenced the genome of the bacteria, finding that it contained elements from two other previously known strains, O104:H4 and EAEC 55989.
O104:H4, which is a rare, enterohemmorhagic - or bloody diarrhea-inducing - strain, has only been documented in scientific literature once before. In 2005, a 29-year-old woman was admitted to a Korean hospital and was treated for the infection and later recovered.
This E. coli represents a new serotype, or sub-species variant for this kind of bacteria. It also has a "shiga toxin," which targets kidney cells and has the ability to enter the blood stream.
The Beijing Genomics Institute team also said on Thursday that the new bacteria has "93 percent sequence similarity" with EAEC 55989, another type of E. coli that is known to have an advanced ability to "colonize" the human stomach - that is, to latch on and reproduce quickly.
I am semi-handicapped here, because I do not totally understand the scientific language; but what I found may hold a tiny clue to the behaviour of bacteria inside and outside the intestines of warm blooded animals and humans.
There is a report from 1961, that may or may not be relevant:
Experimental Genetic Recombination In Vivo Between Escerichia Coli And Salmonella Typhimurium H. Schneider, Samuel B. Formal, and L. S. Baron PDF
I do not know much about the microbiological scientific side; but I do know something about the strange workings of the stomach and large intestine and all its little issues with mold, fungus, yeast and Candida Albicans overgrowth.
I could be wrong .. but perhaps modern medical research spends too much time in mono-hypothisis [I just made that up] .. and this approach leads to a mis-understanding of how things really work in the body.
For example, a micro-biologist may look at cancer cells, fungus, mold, yeast, candida or pathogenic E. coli and bacteria .. but they may not look at how all these micro-organisms interact inside the intestinal environment.
Therefore, E. Coli is E. coli and Candida is Candida .. mold is mold and cancer is cancer. That is what I mean by mono-hypothesis. In the cited 1961 article it states: "In any case, it is felt that the experiments reported here add further to the theory that recombination between organisms plays a role in the natural evolution of the enteric group of microorganisms."
I imagine this is suggesting that enteric microorganisms affect each other and may 'recombine' within the biosphere of the colon (intestines) .. and that we are dealing with a SOUP of organisms who are interrelated and who affect the chemistry of the enteric environment.
For example, all microorganisms have, create and sustain their own chemical environment, in which the bodies immune system has to decide is this beneficial or non-beneficial to the life force of the human, goat, bird, lion and even tree!
The life threatening factor to warm blooded animals and humans could be when a particular microorganism such as E. coli 0104 chemically alters the complete enteric (intestinal) environment. Potentially, altering the acid/alkaline balance and creating multiple complications such as the rapid overgrowth of Candida Albicans (among other things).
Because the 'microbiological detective' is looking for only one cause, they overlook the multiple domino effect of follow on toxins due to a general shift in the intestinal balance. I am thinking that the real devastation may be that the E. coli 0104 pathogen is setting off a much wider chain reaction upsetting many of the intestinal microorganisms (one of which may be Candida Albicans) through chemical changes to the intestinal environment.
The other additional question is why do some people experience more severe symptoms and why do some people experience less severe symptoms? Is it possible that the E. coli strain is altering its behaviour [or severity] depending on the type of microorganisms inhabiting the intestines of the host.
In other words [and I am only guessing], is E. coli 0104 recombining with different strains of intestinal E. coli within the host and in some circumstances recombining with specific varieties of the host E. coli to become more virulent?
Oh! How stupid of me microbiologists already know this! But ... ??
