"Chlamydia enters into cells via abnormalities of key cell membrane receptors, and settles down into anaerobic tissue sites as a mucous-like and sticky matrix where it aggregates, communicates, and constructs slimy edifices called biofilms. (1-7) Because biofilms resonate harmoniously and consist of a dense symbiotic aggregation of microbes embedded in a highly hydrated polymer, polysaccharide matrix of its own secretion, they often end up in the cornea, tonsils, wounds, nasopharynx, middle ear, prostate and urinary tract, teeth (under root canals, fillings, implants, or as chronic bacterial ostitis in extraction sites), dental plaque, oral soft tissues, gall bladder, GI epithelium, heart (endocarditis) and lungs, making them notoriously difficult to treat. Their anti-microbial resistance coupled with the inaccuracy of current lab tests to diagnose hidden biofilms and intracellular infections makes biofilms the greatest clinical challenge facing doctors today. (8-13)"
Free-living amoebae (FLA) are ubiquitous and have been isolated from soil, fresh water, tap water, hydrotherapy and dental equipment, humidifiers, sewage treatment works, and even from dust and the air. FLA feed on bacteria and other micro organisms including fungi, yeasts, algae and other protozoa. They thus have an important ecological role as predators controlling microbial communities."
Free Living Amoebas come in many forms:
I have seen what I have called "crop circle" patterns in my dishes in which the cells of the experiments have age, I have wondered what these patterns have meant:
STARVING AMOEBA: Image of amoeba mitochondria under starvation stress.
"During fasting, the structure of the mitochondria of the free-living giant amoeba (called Chaos carolinense) undergo dramatic changes -- the team wants to determine the role of the cubic transition in response to oxidative stress, the underlying process of ageing and many age-related human diseases."
"Nature is the best teacher. Nature has shown us the structure of some of the most complex of nano or microstructures," said Dr Deng. By looking at the smallest microcosm of nature, we may find solutions. Polymer, a very popular synthetic material in nanotechnology, can self assemble and behave a lot like cubic membranes. The cell membrane, unlike our traditional view of it being a flat sheet, actually nano-periodically folds itself into three-dimensional structures - sometimes folding upon itself in two layers and even as many as 12 layers."
These are giant cells that she is studying which look similar to ours:
REVEALING CELL SECRETS: Dr Deng Yuru has been studying cubic membranes for the last 10 years.
"Dr Deng has been studying cubic membranes for about 10 years. The study has opened for her, peepholes into the labyrinths of nature to reveal their "inner beauty" - an ever changing landscape. Scientists have from as long ago as 1950s, observed the highly organised membrane patterns under transmission electron microscope (TEM), but could not comprehend their 3-D architecture. One theory is that cell membranes react to stresses or stimulants by folding themselves into cubic structures. So far, three such structures have been well studied - based on the mathematically well-defined models, the gyroid (G), double-diamond (D) and primitive (P).
Interestingly, cubic membranes identified in cell organelles share the same geometry of cubic phases studied in many other disciplines such as mathematics, physics, polymer chemistry, and material sciences. Recently much attention has been paid to the multi-continuous cubic phases for their unique physico-chemical features and potential practical uses. In the near future, some of the promising applications of cubic phases will include drug and gene delivery, matrices for membrane proteins crystallisation, and templates for fabricating 3-D band gap photonic crystal materials.
"Through such studies, we gain a better understanding of what's happening within the cell," said Dr Deng.
For example, we may, one day, come out with a new vector, a transporting vehicle for DNA in gene therapy. Virus was used as a vector for carrying the healing DNA to the body where it is needed. But this is not a safe method as the virus has adverse side effects on the patient
The name "cubic membrane" was coined by Dr Deng's supervisor, Professor Tomas Landh in 1994, then at the State University of New York, Buffalo. Dr Landh dug through journals and discovered thousands of published TEM pictures of complex membrane structures that were put aside and treated as anomalies.
Professor Landh has been matching computer generated 2-D projections and electron micrographs and with the help of mathematics, he has come out with the most accurate description ever of the 3-D shapes of cell membranes. He has since joined the commercial sector but Dr Deng and her team at NUS are continuing the study. They are the only ones in this region studying the mechanisms that underlie the formation of cubic membranes. Though there is emerging interest, there are very few scientists around the world who are looking specifically into this area of research.
"The main objective of our research group is to understand the biological functions of cubic membranes, which are mathematically well-defined, 3-D nano-periodic structures occur in a wide variety of living systems," said Dr Deng."
Protochlamydia naegleriophila (nae.gle.rio´.phi.la Gr. fem.n. Naegleria, name of host cell, Gr. adj. philos, -a friendly to, referring to intracellular growth of Protochlamydia naegleriophila strain KNic within Naegleria amebae).
The 16Sr RNA sequence (DQ635609) of KNic is 97.6% similar to that of P. amoebophila, making this organism a member of the genus Protochlamydia. KNic does not grow on axenic media (1) but grows by 4 logarithms in 60 h within A. castellanii. KNic exhibits a Chlamydia-like developmental cycle, with reticulate, elementary, and crescent bodies. The reticulate body is about 900 nm and has a spiny appearance similar to that of P. amoebophila (Figure 2, panel B). To be classified within the Pr. naegleriophila species, a new strain should show a 16Sr RNA similarity >98.5% (13) and similar phenotypic traits."
**Barb, look at the pattern of "A"?... doesn't this look similar to what you're posting in your photos? I have photos of some of these patterns, I didn't have a clue as to what I was looking at, I will find them.
We know that Dr. Martin found a high number of Morgellons patients tested positive for C. pneumonia? I have looked for a link to his reporting this and cannot find it any longer, I believe it was 92%, can anyone find it? Martin's information might have been from where Carnicom drew his conclusions?
I thought this was a very good article that I just found while looking:
Step 1 - Ask your doctor to test you for Chlamydia pneumoniae. Researchers have associated a high number of Morgellons patients with these bacteria. Treatment includes 6 months to 3 years of amoxicillin, N-acetyl cysteine, doxycycline and azithromycin.
Step 2 - Get tested for Lyme disease. Researchers have linked Morgellons disease to Lyme disease, and many Morgellons patients have had a positive Lyme titer. Doctors treat Lyme disease with tetracycline, penicillin, cephalosporin and erythromycin.
Step 3 - Learn if you harbor Babesia microti, a protozoan associated with Lyme disease infection. It causes the joint pain, fatigue and shortness of breath many Morgellons patients experience. Treatments include clindamycin, quinine, atovaquone and azithromycin."
When several pathogens that produce a biofilm vie for an area this is called a "biofilm swarm" and have what is known as "swarm intelligence", which I believe is happening and is most likely a specific process in our case with the like-pathogens we have in common.
"Decision-making between rapidly colonizing a surface and biofilm formation is central to bacterial survival among competitors."
I found this abstract where they tried to stop a BS swarm which we also believe to be involved, we just noted yesterday where the marine and red algaes might be helpful supplements in breaking up the biofilm and quorem sensing aspect, that possibly breaking up the biofilm and quorem sensing might be a good place to start in attacking the other pathogens:
"Inhibition of biofilm formation and swarming of Bacillus subtilis by (5Z)-4-bromo-5-(bromomethylene)-3-butyl-2(5H)-furanone
Aims: (5Z)-4-Bromo-5-(bromomethylene)-3-butyl-2(5H)-furanone(furanone) of the marine alga Delisea pulchra was synthesized, and its inhibition of swarming motility and biofilm formation of Bacillus subtilis was investigated.
Methods and Results: Furanone was found to inhibit both the growth of B. subtilis and its swarming motility in a concentration-dependent way. In addition, as shown by confocal scanning laser microscopy, furanone inhibited the biofilm formation of B. subtilis. At 40 μg ml−1, furanone decreased the biofilm thickness by 25%, decreased the number of water channels, and reduced the percentage of live cells by 63%."
We also see where The natural furanone (5Z)-4-bromo-5-(bromomethylene)-3-butyl-2(5H)-furanone disrupts quorum sensing:
"Emended description of the order Chlamydiales, proposal of Parachlamydiaceae fam. nov. and Simkaniaceae fam. nov., each containing one monotypic genus, revised taxonomy of the family Chlamydiaceae, including a new genus and five new species, and standards for the identification of organisms"
Let me look at the species and family mentioned to see if any of them resemble what we're seeing microscopically or if I can find newer articles with more additions to these findings. From this article we can see that a "sister" Simkaniaceae contains a "cousin" species names Simkania negevenis. So, if Simkaniaceae is a "sister", then Waddlia, Neochamydia, Parachamydia, and Chamydophila are, too. Our pathogens might be one of these or one not identified yet, we can see the family tree in this diagram below in Figure 1., feel free to help me look. In my research, I also saw a reference to "Protochlamydia", which I'm not sure where it fits in?
"The current taxonomic classification of Chlamydia is based on limited phenotypic, morphologic and genetic criteria. This classification does not take into account recent analysis of the ribosomal operon or recently identified obligately intracellular organisms that have a chlamydia-like developmental cycle of replication. Neither does it provide a systematic rationale for identifying new strains. In this study, phylogenetic analyses of the 16S and 23S rRNA genes are presented with corroborating genetic and phenotypic information to show that the order Chlamydiales contains at least four distinct groups at the family level and that within the Chlamydiaceae are two distinct lineages which branch into nine separate clusters."
** Where is the rRNA testing data for our chlamydia-like organism? Why hasn't this been done to date and published?
"In this report a reclassification of the order Chlamydiales and its current taxa is proposed. This proposal retains currently known strains with > 90% 16S rRNA identity in the family Chlamydiaceae and separates other chlamydia-like organisms that have 80--90% 16S rRNA relatedness to the Chlamydiaceae into new families."
**These rRNA numbers will tell us where our organism belongs in this family.
"Chlamydiae that were previously described as ‘Candidatus Parachlamydia acanthamoebae’ Amann, Springer, Schönhuber, Ludwig, Schmid, Müller and Michel 1997, become members of Parachlamydiaceae fam. nov., Parachlamydia acanthamoebae gen. nov., sp. nov. ‘Simkania’ strain Z becomes the founding member of Simkaniaceae fam. nov., Simkania negevensis gen. nov., sp. nov. The fourth group, which includes strain WSU 86--1044, was left unnamed."
**WSU 86--1044?... left unnamed in 1999... ?? What is its name today, what are its characteristics?
"The Chlamydiaceae, which currently has only the genus Chlamydia, is divided into two genera, Chlamydia and Chlamydophila gen. nov. Two new species, Chlamydia muridarum sp. nov. and Chlamydia suis sp. nov., join Chlamydia trachomatis in the emended genus Chlamydia. Chlamydophila gen. nov. assimilates the current species, Chlamydia pecorum, Chlamydia pneumoniae and Chlamydia psittaci, to form Chlamydophila pecorum comb. nov., Chlamydophila pneumoniae comb. nov. and Chlamydophila psittaci comb. nov. Three new Chlamydophila species are derived from Chlamydia psittaci: Chlamydophila abortus gen. nov., sp. nov., Chlamydophila caviae gen. nov., sp. nov. and Chlamydophila felis gen. nov., sp. nov. Emended descriptions for the order Chlamydiales and for the family Chlamydiaceae are provided. These families, genera and species are readily distinguished by analysis of signature sequences in the 165 and 235 ribosomal genes."
**Some of the family members to investigate. We can see how two or three of these different Chlamydophila are coming together to form a new species? This might explain how we are seeing 'spheres' that appear similar but are preforming different duties, reproducing differently and that we have a combination of 4 or more happening inside our disease?
I need a more current report to see what has developed since 1999.
Development of Batrachochytrium dendrobatidis zoospores.
The name of the photograph above is "ChytridDevelopment.png", this suggests that this is how the Chytrid species develops overall?
Below is a comparison from human ear lesion, cultured in nutrient agar at 30 days growth at 100x:
I'm noticing that there aren't too many good microscopic stock photos, but this one above is a good example to give us an indication that Batrachochytrium dendrobatidis or a Chytrid fungus species is most likely involved as one of the mystery Morgellons fungi.
Literature says, "Chytrids will not infect human skin since they do not multiply above 31° C." something is definitely happening in my ear lesion photo above and it's above 31 degrees C (87.8 F)! A hybrid?
Well... what does all of this mean, is this the big secret behind Morgellons Disease? The animal species are being attacked by environmental factors to create disease, wipe-out of large populations, etc. - up the chain, the frog disease has transmitted to man worldwide? What does this information suggest on a global scale?
We can see that millions of dollars have been spent studying the frog disease, these scientists hopefully have some answers that they can easily transfer over to the medical professionals in regard to how the fungal and chlamydial aspect of the frog's disease is manifesting itself inside of Morgellons Disease.
Now, it's just a matter of blood testing or skin through biopsies to match to the frog's pathogens, to get this information into the right hands and let it be verified or dismissed.
It's not JUST "the frog disease" we have, this thread is about the hidden aspect - the frog chlamydia and fungus doesn't begin to explain the insects coming out of our skin! What made the koala, frog, reptiles, bats sick?... this is a small fly-nematode/water disease, that's the hidden part, that's what I've been calling the "baculorviral aspect" and showed how it is happening inside the chlamydia or fungal spheres (to be studied).
The question is... How did it get in there to begin with? and... How do we stop it?... AND... the U.S. Army is going to tell you all about this... any day now.
(The puzzling part to me is... I can see how all of these animal species that have become sick are in contact with the gnat/nematode, but... the bees and butterflies?...)
it opened a lot of doors for me - we now have names for some of the artifacts we've been seeing and proves some of the theory that we have proposed is most likely happening, such as; we have HeLa cells, photos to show this aspect later.
Fig 2. A Chlamydia trachomatis elementary body (EB) in the process of entry into a HeLa cell. Tannic acid stained to enhance visualisation of chlathrin. Note the clearly demarcated outer envelope of the EB and the surrounding membrane (m) of the vacuole. Also note how small the clathrin coated pit (ccp) is compared to the chlamydial endosome. The bar represents 0.1 microns.
We now have a name for our 'carbon-looking balls':
The 'balls' that are inside of the fungus gnat larvae @100x:
The same ones inside of our nematodes, Urine at 600x:
They are called a clathrin coated pit, labeled "ccp" in the diagram above.
If we research the clathrin coated pit, we see how certain fibers form these spheres:
Reconstitution of Clathrin-coated Pit Budding from Plasma Membranes
Here's the problem. For some reason it has been published that this Chytrid Fungus will not affect humans because it will not grow in above 31 degrees C. or 88.7 F. temperatures.
I don't know who published this information but it has kept us with Morgellons away from looking at the frog's illness being related to ours. This is Morgellons Disease... anything is possible!
Since the frog's dying is a big issue - there are many labs that will allow you to rub a swab across the tummy of your frog and mail the swab in for a PCR test. I'm going to swab my ear and send it in like my ear is a frog and see how the lab test comes back.
There's a list of labs that will do this at the bottom of this article:
"I believe this is what happened in nature and for us to become infected by animal- and plant pathogens:
An alternative explanation for virulence in microbes acquired from the environment is cryptic pathogenesis, whereby such microbes have animal hosts that are yet to be discovered.
In such a scenario, some fraction of the microbial population is always cycling through an animal host, and consequently, attributes for persisting in animal hosts are maintained through selection.
The finding that land and marine mammals in areas where Coccidioides immitis is endemic are sometimes found to be infected with this fungus is consistent with a cryptic-pathogenesis explanation.
Although the possibility of cryptic pathogenesis cannot be excluded for any environmentally acquired microbe, since this would involve proving a negative, there is experimental evidence against an absolute need for animal passage in the maintenance of virulence.
Avirulent strains of C. neoformans and H. capsulatum can be restored to virulence through passage in the amoeboid hosts Dictyostelium and Acanthamoeba castellanii, respectively"
We don't have any indication that Morgellons Disease was deliberately set upon us, we can start a conspiracy thread over in the Theories section?
So far, with our limited resources - we're seeing that Morgellons is an extension of cancer, a benign pseudo-cancer, giant cell granuloma, that is why when we are tested our results show 'atypical cells' or 'giant cell involvement' and not necessarily cancer. These cancer-causing organisms have been around for years - but, not in our existing form. Morgellons is a mistake that even the scientists creating their individual parts of our disease could not predict as Jeany's (Katinka's) last post explains - cryptic (hidden) pathogenosis from inert pathogens coming alive from global warming, ice melting, ships passing the pathogens around the world from their bilge waters... etc., bringing together amoeba and fungi that have been asleep, when put together become awake, etc. So far, that's what we're seeing, the unpredictable has happened.
Why would any Government want to mind control a large segment of the population by re-wiring them to control them when they are riddled with disease, consumed by their illness, are showing the signs of bi-polar, ADD... and the list goes on... on the negative side of the ledger book - what advantage is a sick army? Every good military man knows that it takes at least three able men to take care of one injured one. We are a liability to our Government, not an asset, IMO we represent a combination of several lab mistakes intertwined with the existing natural world of pathogens.
"There are many different kinds of bacteria but only one type that has been consistently observed and studied in cancer for over a century. The cancer microbe has many forms, some of which appear as ordinary staphylococci or larger yeast-like forms that further enlarge to the size of Russell bodies. As mentioned, some Russell bodies enlarge to truly gigantic proportions, one hundred times the diameter of small cocci. One can liken this growth potential to an empty balloon that is then blown up to full-size. In addition, the microbe has exceedingly small filterable submicroscopic forms approaching the size of viruses, visible only by use of the electron microscope.
The mystery of these “yeast-like” bodies deep in his skin was solved years later when I first learned about the existence of “large body” forms of Mycobacterium tuberculosis. When this patient died, Mycobacterium fortuitum, an “atypical” form of mycobacteria was cultured from his scleroderma tissue.
In 1981 King and Eisenberg’s article on “Russell’s fuchsin body: ‘The characteristic organism of cancer’ ” appeared in the American Journal of Dermatopathology. They reconfirmed that “Russell bodies have now been shown to be immunoglobulins.” They remarked that Russell was not the first to describe them; and that similar bodies were reported by Cornil and Alvarez in rhinoscleroma five years earlier in a French journal in 1885."
I was looking at photos for Kat and saw this one of the inside of what I have called the "steering wheel" in the past. It is huge in size, this is 1/6th of the sphere, it goes all the way around and makes a 'wheel' with these 'spokes' that lead from the center 'hub'. I have quite a few of this phenomena in a couple of different human experiments, that shows what it looks like all the way around the 'wheel'. It has an irredentist, metallic rainbow-colored sheen to it. I'm not sure what it means? It reminded me of how the clarthin vesicles are formed, though.
I believe it shows the beginning signs of a sphere that is in a 'starving' state because this is 45 days into the experiment where the Petri Dish is drying or running out of nutrients, Human lesion, 45 days @ 300x:
It reminds of this pattern found in clathrate hydrate:
Ok, Jeany we already know that we can closely implicate H. capsulatum that's more verification along with the "Dicty", as per Jan Smith's research, to show that this cryptic pathogenesis has most likely happened. (See the one in the background of the Dr. Fungus photo looks like it's forming the 'spokes'?)
Histoplasma capsulatum looks like everybody else named recently in its early development stages, except - we can see one stock photo in particular that gives us a good clue that this guy is most likely involved with some of us? This photo shows what it looks like in a more mature, budding state of development from Dr. Fungus:
I amy be wrong but I believe the sphere is what starts the whole construction of this.
Do you think the sphere itself is what is inorganic?
That could be from the archaea or nanoarchaean and the volcanic symbiosis.
The rock itself.
Two that are symbiotic are these.
on the nano bacterium thread.
Of course, I have wondered if the spheres, which appear to all look the same starting out:
appear to preform similiar within the ones that are alike, such as the ones that turns into the white or black, fuzzy fungus balls... they transform consistently the same way over and over, and yet the 'others' that are not turning into 'fungus-balls' appear random and morphed depending on the other pathogens that are in their vicinity, or possibly what illnesses the person has? I have thought the fungi is inorganic because it has not been seen nor identified yet. I recently learned that the way that traditional labs analyze for fungi, ours could easily be missed.
I have researched the various containers that our pathogens could be in, it is possible that we have one container, a man-made inorganic vesicle or micelle? It's hard to say - I am almost positive that the above spheres that comes out of the gnat larvae turns into the same artifacts that are seen below in humans. This life cycle is consistent in that the same artifacts found in humans, insects, red wine, certain foods, tap water, cotton products, paper, etc. ALL show the same Morgellons artifacts eventually in the Petri Dish.
The membrane of our sphere walls would have to be analyzed by the proper equipment to gather their physical chemical composition. It seems that whatever their composition, if they are an inorganic material, would show up in a Blast test? If the cell membranes were all the same inorganic material, to me, this would indicate something different.
Here's a progression study that I did where I took some lesion debris from my ear and put it into the Petri Dish, it doesn't isolate any particular particle, it just shows the diversity of what's possible to happen from body debris after 5 days:
I chose the 'carbon ball' as the beginning of the life cycle because, it ends up coming out of the organisms as frass and starts the whole process all over again. They are producing the frass/fibers while they are in their larvae stages and when they become adults, the only explanation is that if a gnat (the nematodes are also seen inside the gnat larvae, and appear to replicating via this 'carbon ball' technology independent of the gnat, also) is created from a 'bucky ball' - a baculoviral aspect has to be involved?
Look at this Life Cycle closer, it scares the beezus out of me. Even if the gnat larvae doesn't make it to adulthood, it is still defecating the carbon balls while it is going through its instars. Any water that the gnat touches becomes contaminated with the 'Morg' pathogens.
I have photographed another organism that resembles a tomato hornworm in its larval stage, I'm thinking it is actually the fungus gnat larvae also. Some of the others are showing signs of Schistosoma mansoni involved in their disease. And, then others will say they have seen or have other organisms... what all is actually involved, is inconclusive at this time or even if these are real or "expressions" (the DNA of one thing expressed to simply hold or house another), such as the 'shell' aspect. The fungus gnat and nematode are real - in that they are the end products of the other's "expressions", as in a baculoviral expression.
AND... we're not just talking about just the gnat and nematode here, as we're looking closer we're seeing most all of the insects and animals are affected in some way or another, their pathogens are matching ours - the koala, frog, bees - their mites, bats, snakes, our natural body mites?... etc., etc. - I'm saying that I believe Morgellons started with the fungus gnat being manipulated because it appears to be the end product, the nematode and others are along for the ride or were present or acquired after the fact and were incorporated into the 'system'.
Another possibility is that there are two or more strains of Morgellons in which one contains the Schistosoma mansoni or expression thereof and the other one does not? Or, this Schistosoma factor or expression is hidden and not known until many years into the disease and is present in all?
tash: Hi skizit, I have watched all your videos on youtube and cant thank you enough for all you have educated me on. I cry for you alot and a bit for me. I was wanting to send you photos of what is raining down everyday here in Australia in hope you can tell me
Dec 11, 2019 23:28:22 GMT -5
tash: not sure where to send them as hush mail and rocket mail bounced back
Dec 11, 2019 23:30:03 GMT -5