Mycoplasma Pneumonia (Eaton Agent)
[Be sure to click on all the hot links to see the pictures]
Eaton agent, the microbe that has been associated with atypical pneumonia, was originally thought to be a virus because certain antibiotics were not effective and it was so much smaller than cell wall form bacteria.† It was found to have one of the smallest genomes among bacteria and belongs to the Class: Mollicutes, Order: Mycoplasmatales, Genus: Mycoplasma, Species: Pneumoniae.† Mycoplasma Pneumonia.† A related Mycoplasma is M. hominus that Drs Brown and Clark associated with rheumatic arthritis. Clarkís pictures are of M. hominis, not M. pneumonia† (MP).
MP was found to be sensitive to gold salts, and tetracyclines, both of which are useful treatments for arthritis and other rheumatic conditions.† It is not sensitive to antibiotics that attack cell walls. Penicillins and other beta-lactam antibiotics.† It is sensitive to macrolides (erythromycin, azithromycin, clarithromycin), fluoroquinolones and their derivatives (e.g., ciprofloxacin, levofloxacin), and tetracyclines (e.g., doxycycline).
The detailed structure is depicted in M. pneumonia genetic summary† reported by NewScientist with a detailed electron-tomograph picture showing remarkable detail in color. That picture of M. pneumonia bacteria shows smaller body components, like ribosomes, chromosomes, or mitochondrial organelles that bound and enable molecular chemical transformations in host cells, driven by the DNAsí, RNAsí and now XNAsí recipe-templatesí codons. †MP invades epithelial cells in the respiratory tract and contributes to COPD respiratory inflammation and bronchitis. MP invades erythrocytes (RBCs) and also invades immune cells, (phagocytes) leading to suppression of immune functions.† Invaded host epithelial and blood cells act as replication factories for the obligate microbes, similar to the way viruses replicate.
The ring like shapes inside the MP cell membrane in the electron tomograph resemble the M. hominis ring shapes pictured by Harold Clark. [Page 13] His Figure 4A structure size 100,000 magnification and ~.5 micron donut shape diameter with hole of about .25 micron diameter.
Pathology is complex for M. pneumonia, other Mycoplasmas (M. hominis, fermentans, et al),† and other persistent, obligate microbes.† The first order symptomology of MP is pneumonia, bronchitis and COPD.† Since MP is persistent, COPD is episodic. Since the human herd is near 100% infected by Chlamydia pneumoniae,† and RSV (respiratory syncytial virus) the other persistent microbes can† all work together to infiltrate immune cells, to suppress immune system functions and to infect/invade† blood and epithelial cells in various other parts of the body.
A wide spectrum of rheumatic conditions are linked to MP as a co-factor,
∑ Alzheimerís disease, Amyotrophic Lateral Sclerosis (ALS), Arthritis Asthma, Arterial sclerosis, Atypical pneumonia, Bronchitis, Cardiovascular diseases, CFS/CFIDS, Crohnís diseases, COPD, fibromyalgia syndrome (FMS), Interstitial cystitis, Leukemia, Lymphoma, Lupus (SLE), Multiple sclerosis (MS), Pelvic inflammatory disease (PID), Psoriasis, Scleroderma,† Solid (&lung) cancers, Sjogrenís syndrome,.
∑ Mycoplasmas can change in nerve conduction, demyelation (a degenerative process that erodes away the myelin sheath that normally protects nerve fibers) and sensitivity.
∑ Mycoplasmas can also disrupt the hostís immune system. They can stimulate lymphocytes to secrete inflammatory cytokines, which lead to inflammation and both stimulation and/or suppression of the immune system.
∑ Mycoplasmas leaving an infected cell incorporate hostís cell surface material into their own surface structure, they can instigate an autoimmune response. Meanwhile the emerging mycoplasmas can evade the immune system by hiding inside host cells or fusing with the host cellular membranes.
∑ Pathogenic mycoplasmas can also invade lymphocytes and disrupt their functioning, provoking defective immune responses. Using molecular mimicry, mycoplasmas can even closely replicate host cellsí surface structures to resemble normal host cells.
∑ After invading host cells, mycoplasmas can trigger the release of reactive oxygen free-radicals (ROS) that modify the RNA and DNA of the cells, leading to malignant cellular transformations without apoptosis. Benign (non-cancerous) cells infected by mycoplasmas became irreversibly malignant (cancerous) after 18 cell divisions.
Drs. Nicolson, See and Akbarpour, of the Immune Institute in Huntington Beach found ~90% of certain late stage cancer patients have mycoplasma infections. Mycoplasmas increase the progression growth rate of cancer cells.
Mycoplasmas can also invade the epithelial lining of blood vessels, where they appear to facilitate the release of molecules that can cause vasculitis (inflammation) and the formation of plaque inside blood vessel wall surfaces. In the absence/shortage of protecting vitamin C and Lysine† See Pauling Case History.
Mycoplasmas Shape Change to multiple forms:
Mycoplasmas and other persistent microbes are equipped to change shapes and form, appearing then disappearing, changing shape, shuffling their surface elements, invade host cells, then hang out as normal flora coated with molecules taken from the cells they invaded. They even have protective forms to defeat antibiotics and some can shift to this form in a few short minutes as seen in vitro under a microscope.† Pulsing the antibiotic can multiply-attrite the shape-changing microbes, but this pulsing protocol is not widely followed. It should be.
MP are pleomorphic (structurally changing). In place of rigid cell walls, they have flexible lipid (water insoluble fat) outer surfaces. Like amoebas they bend and move, squeezing into tight spaces. They are so small they slide through laboratory and hospital filters used to produce or maintain bacterial sterility -- making them one of the most common contaminants in diagnostic laboratories and vaccine manufacturing.
Mycoplasmas Contaminate other Vaccines:
They grow in the same live cell media used to grow virus vaccines.† In one recent study of vaccines, mycoplasmas were found to contaminate about six percent of commercial vaccines.† As contaminants of both live and killed vaccines, their presence can generate an unintended immune response.
Past trials of experimental M. pneumonia vaccines were reported as dangerous failures. The tested MP vaccines both did not protect, but they also generated a significant fraction of life-threatening, very strong immune/inflammation reactions to the wild mycoplasma test challenge forms. So mycoplasma †vaccine contamination makes the vaccines dangerous for a significant† (~5%) fraction of those inoculated. Total risk factor is .05*.06= .003 or .3% or 3 in 1000 cases.† Live MMP vaccines contaminated with mycoplasmas, †can infect the vaccinated. Cases of infected live virus vaccines documented in the literature include contamination with HIV, SIV, parvovirus, measles, smallpox and polio strains that lead to
Mycoplasmas infect everything including animals, plants, and possibly other microbes. Generally, strains have adapted to specific host species, with some exceptions. Garth Nicolson the pets of GWI or CFS patients exhibited similar symptoms as their owners, and then tested positive for the same mycoplasmas. They are highly contagious, but not all infected show noticeable symptoms. Transmission occur among people in close proximity (families, classmates, etc).
Mycoplasmas invade the cells of the host (patient) and oror to attach-to or imbed-into the outside of host cells.
They depend on host cells for nutrients such as cholesterol, certain amino acids, etc. They compete with the host cells for these nutrients and energy which can interfere with host cell functions. Fatigue is one symptom.
†A mycoplasma has very little DNA of its own, but is capable of using/controlling DNA from an invaded cell causing that cell to malfunction in many significant ways (mitochondrial dysfunction) and/or die, or invasion can cause inflammation and DNA/RNA mutation and damage of the host cells.
†Mycoplasmas attach to host cells with a tiny arm coated in protein which attaches to the protein coating of host cells. For this reason, antibiotics like tetracycline, which are classified as "protein synthesis inhibitors" are often used against mycoplasma infections. While these antibiotics may block this protein attachment and very slowly starve it from the nutrients it needs from host cells to thrive and replicate, it still takes a healthy immune system to actually kill the mycoplasma for good. Better nutrition, especially vitamin C in high consistent levels, can stimulate invaded cell apoptosis (death).
†Mycoplasmas are highly adaptable to changing environments and can move anywhere in the body, attaching to or invading virtually any type of cell in the body that has a shape that matches the form of its protein hooks.
†The mycoplasma adhesion proteins are very similar to human proteins. Once adhered to the host cell, the mycoplasma can completely mimic or copy the protein cell of the host cell. This can cause the immune system to begin attacking the body's own cells, diagnosed as an autoimmune disease.
†Certain Mycoplasma species can either activate or suppress host immune systems, and they may use these activities to evade host immune responses. Mycoplasmas can turn on the chain reaction immune responses. This includes the generation of pro-inflammatory cytokine molecules which are found in inflammatory disorders, called autoimmune diseases.
†Mycoplasma can signal and attract immune system phagocytes (natural killer NK cells) that are supposed to eat them. Inside these phagocytes, they can make copies of themselves and† be carried to new locations of inflammation.
†When a mycoplasma attaches to a host cell, it generates and releases hydrogen peroxide and superoxide Nitrogen and Reactive Oxygen Species, AKA free-radicals, (NOS and ROS) and these (hy)peroxides damage cells organs, tissues, mitochondria, and DNA/RNA, aging the host.† Vitamin C is the antidote.
Mycoplasmas - Stealth Pathogens By Leslie Taylor, ND†† January, 2001
Concise web MP Tutorial by Travis Wojtowicz: see
∑ M. Pneumonia;†