The number of known conditions in which mycoplasmas play a role is growing, thanks to advances in detection. Mycoplasmas are now said to be contributors, or at least cofactors, in a number of conditions, including CFS/CFIDS, fibromyalgia syndrome (FMS), lupus, multiple sclerosis (MS), psoriasis, scleroderma, Chrohn’s diseases, solid cancers, leukemia, lymphoma, Amyotrophic Lateral Sclerosis (ALS), pelvic inflammatory disease (PID), asthma, atypical pneumonia, Sjogren’s syndrome, interstitial cystitis, Alzheimer’s and cardiovascular diseases. Mycoplasmas have also been associated with a variety if autoimmune diseases that can cause definite changes in nerve conduction, demyelation (a degenerative process that erodes away the myelin sheath that normally protects nerve fibers) and sensitivity.

Immune Disruption

Mycoplasmas can also disrupt the normal orchestration and organization of the host’s immune system. They can cause lymphocytes (white blood cells that bear the major responsibility of the immune system) to secrete inflammatory cytokines (proteins that facilitate cell-to-cell communication), which leads to swelling, inflammation and either stimulation or suppression of the immune system.

Because pathogenic mycoplasmas leaving a cell they have infected can incorporate much of the host’s cell surface material into their own surface structure, they can instigate an autoimmune response in which the immune system starts attacking the host’s own cells, a process that can result in severe tissue damage and pain.

Meanwhile the mycoplasmas evade the immune system by hiding inside host cells or fusing with the cellular membrane of the host cells. Certain pathogenic mycoplasmas can also invade lymphocytes and disrupt their functioning without provoking an immune response. Using a trick known as ‘molecular mimicry,” mycoplasmas can even closely resemble host structures to fool the immune system into thinking that they are normal host cells.

After invading host cells, mycoplasmas can trigger the release of “reactive oxygen” free radicals that modify the RNA and DNA of the cells, an event that can eventually lead to malignant transformation. This phenomenon has been observed in a laboratory study in which benign (non-cancerous) cells infected by mycoplasmas became irreversibly malignant (cancerous) after 18 cell divisions. Dr. Nicolson has been working with two colleagues, Drs Darryl See and Ferre Akbarpour, of the Immune Institute in Huntington Beach. Their research has found that nearly 90% of certain late stage cancer patients show infection with pathogenic mycoplasmas. These mycoplasmas appear to drive the progression of cancer cells, making them more malignant and metastatic (capable of spreading throughout the body).

Mycoplasmas can also invade the lining of blood vessels, where they appear to facilitate the release of biochemicals that can cause vasculitis (inflammation of blood vessels due to infection) and the formation of plaque inside blood vessel wall surfaces.

How Mycoplasmas Operate

Mycoplasmas are well equipped to play biological sleight-of-hand, appearing then disappearing, changing shape, shuffling their surface components, ducking into cells, then parading as normal citizens of the human flora dressed in clothes stolen from the cells they invaded. They’re elusive because they are pleomorphic (structurally changing). They do not have rigid cell walls like most bacteria; instead they possess fluid lipid (water insoluble fate) outer surfaces, and like tiny jellyfish, they can squeeze, bend and move into tight spaces. They can also slide right through laboratory and hospital filters used to produce or maintain sterility – making them one of the most common contaminants in diagnostic laboratories and vaccine manufacturing. In one recent study of vaccines, mycoplasmas were found to contaminate about six percent of commercial vaccines.

These microorganisms have been quite successful in adapting to many environments, infecting everything from insects to elephants, plants to people. Generally, they are species-specific, but there appear to be many exceptions. Garth Nicolson relates more than one case in which the pets of GWI or CFS patients were exhibiting similar symptoms as their owners, and then tested positive for the same mycoplasmas. No one knows for sure how contagious mycoplasmas are, but it appears transmission may occur among infected people in close proximity for extended periods of time.

Not everyone who is exposed becomes sick. For example, when Nicolson studied Gulf War veterans’ families who became sick with symptoms similar to GWI, he found that not every member of the family became sick, but those that did become ill had the same infection as found in the sick veteran.

HOW MYCOPLASMAS INTERACT IN THE BODY

Mycoplasmas are able to hide inside the cells of the host (patient) or to attach to the outside of host cells.

Whether they live inside or outside the host cell, they depend on host cells for nutrients such as cholesterol, amino acids, etc. They compete with the host cells for these nutrients which can interfere with host cell function without killing the host cell.

A mycoplasma has very little DNA of its own, but is capable of using DNA from a host cell. When a mycoplasma takes over the DNA of the host cell, anything can happen - including causing that cell to malfunction in many different ways and/or die, or can cause DNA mutation of the host cell.

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.

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.

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; an event that happens in all autoimmune diseases.

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 called an immune system response. This includes the stimulation of pro-inflammatory cytokines (chemical messengers of the immune system) which is generally found in most autoimmune and inflammatory diseases and disorders.

Mycoplasma can also attach to or invade immune system cells, like the very phagocytes (natural killer cells) that are supposed to kill them. Inside these phagocytes, they can be carried to new locations of inflammation or disease - hidden away like a spy who has infiltrated the defending army.

When a mycoplasma attaches to a host cell, it generates and releases hydrogen peroxide and superoxide radicals which cause oxidative stress and damage to the surrounding tissues.

Mycoplasmas - Stealth Pathogens

By Leslie Taylor, ND

January, 2001

Mycoplasmas are a specific and unique species of bacteria - the smallest free-living organism known on the planet. The primary differences between mycoplasmas and other bacteria is that bacteria have a solid cell-wall structure and they can grow in the simplest culture media. Mycoplasmas however, do not have a cell wall, and like a tiny jellyfish with a pliable membrane, can take on many different shapes which make them difficult to identify, even under a high powered electron microscope. Mycoplasmas can also be very hard to culture in the laboratory and are often missed as pathogenic causes of diseases for this reason.

The accepted name was chosen because Mycoplasmas were observed to have a fungi-like structure (Mycology is the study of fungi - hence "Myco") and it also had a flowing plasma-like structure without a cell wall - hence "plasma". The first strains were isolated from cattle with arthritis and pleuro-pneumonia in 1898 at the Pasteur Institute. The first human strain was isolated in 1932 from an abscessed wound. The first connection between mycoplasmas and rheumatoid diseases was made in 1939 by Drs. Swift and Brown. Unfortunately, mycoplasmas didn't become part of the medical school curriculum until the late 1950's when one specific strain was identified and proven to be the cause of atypical pneumonia, and named Mycoplasma pneumonia. The association between immunodeficiency and autoimmune disorders with mycoplasmas was first reported in the mid 1970s in patients with primary hypogammaglobulinemia (an autoimmune disease) and infection with four species of mycoplasma that had localized in joint tissue. Since that time, scientific testing methodologies have made critical technological progress and along with it, more mycoplasma species have been identified and recorded in animals, humans and even plants.

While Mycoplasma pneumonia is certainly not the only species causing disease in humans, it makes for a good example of how this stealth pathogen can move out of it's typical environment and into other parts of the body and begin causing other diseases. While residing in the respiratory tract and lungs, Mycoplasma pneumonia remains an important cause of pneumonia and other airway disorders, such as tracheobronchitis, pharyngitis and asthma. When this stealth pathogen hitches a ride to other parts of the body, it is associated with non-pulmonary manifestations, such as blood, skin, joint, central nervous system, liver, pancreas, and cardiovascular syndromes and disorders. Even as far back as 1983, doctors at Yale noted:

"Over the past 20 years the annual number of reports on extrapulmonary symptoms during Mycoplasma (M.) pneumoniae disease has increased. Clinical and epidemiological data indicate that symptoms from the skin and mucous membranes, from the central nervous system, from the heart, and perhaps from other organs as well are not quite uncommon manifestations of M. pneumoniae disease."(15)

This single stealth pathogen has been discovered in the urogenital tract of patients suffering from inflammatory pelvic disease, urethritis, and other urinary tract diseases (8) It has been discovered in the heart tissues and fluid of patients suffering from cardititis, pericarditis, tachycardia, hemolytic anemia, and other coronary heart diseases.(9, 10, 14) It has been found in the cerebrospinal fluid of patients with meningitis and encephalitis, seizures, ALS, Alzheimer's and other central nervous system infections, diseases and disorders.(11-13) It has even been found regularly in the bone marrow of children with leukemia.(16-18) It is amazing that one single tiny bacteria can be the cause of so many seemingly unrelated diseases in humans. But as with all mycoplasma species, the disease is directly related to where the mycoplasma resides in the body and which cells in the body it attaches to or invades.

Today, over 100 documented species of mycoplasmas have been recorded to cause various diseases in humans, animals, and plants. Mycoplasma pneumonia as well as at least 7 other mycoplasma species have now been linked as a direct cause or significant co-factor to many chronic diseases including, rheumatoid arthritis, Alzheimer's, multiple sclerosis, fibromyalgia, chronic fatigue, diabetes, Crohn's Disease, ALS, nongonoccal urethritis, asthma, lupus, infertility, AIDS and certain cancers and leukemia, just to name a few.(1-6) In 1997, the National Center for Infectious Diseases, Centers for Disease Control and Prevention's journal, Emerging Infectious Diseases, published the article, Mycoplasmas: Sophisticated, Reemerging, and Burdened by Their Notoriety, by Drs. Baseman and Tully who stated:

"Nonetheless, mycoplasmas by themselves can cause acute and chronic diseases at multiple sites with wide-ranging complications and have been implicated as cofactors in disease. Recently, mycoplasmas have been linked as a cofactor to AIDS pathogenesis and to malignant transformation, chromosomal aberrations, the Gulf War Syndrome, and other unexplained and complex illnesses, including chronic fatigue syndrome, Crohn's disease, and various arthritides."

Mycoplasmas, unlike viruses, can grow in tissue fluids (blood, joint, heart, chest and spinal fluids) and can grow inside any living tissue cell without killing the cells, as most normal bacteria and viruses will do. Mycoplasmas are frequently found in the oral and genito-urinary tracts of normal healthy people and are found to infect females four times more often than males, which just happens to be the same incidence rate in rheumatoid arthritis, fibromyalgia, Chronic Fatigue and other related disorders.(7) Mycoplasmas are parasitic in nature and can attach to specific cells without killing the cells and thus their infection process and progress can go undetected. In some people the attachment of mycoplasmas to the host cell acts like a living thorn; a persistent foreign substance, causing the host's immune defense mechanism to wage war. This allergic type of inflammation often results in heated, swollen, and painful inflamed tissues, like those found in rheumatoid diseases, fibromyalgia and many other autoimmune disorders like lupus and MS, Crohn's and others. In such cases the immune system begins attacking itself and/or seemingly healthy cells. Some species of mycoplasmas also have the unique ability to completely evade the immune system. Once they attach to a host cell in the body, their unique plasma and protein coating can then mimic the cell wall of the host cell and the immune system cannot differentiate the mycoplasma from the body's own host cell.

Mycoplasmas are parasitic in nature because they rely on the nutrients found in host cells including cholesterol, amino acids, fatty acids and even DNA. They especially thrive in cholesterol rich and arginine-rich environments. Mycoplasmas can generally be found in the mucous membrane in the respiratory tract. They need cholesterol for membrane function and growth, and there is an abundance of cholesterol in the bronchial tubes of the respiratory tract. Once attached to a host cell, they then begin competing for nutrients inside the host cells. As nutrients are depleted, then these host cells can begin to malfunction, or even change normal functioning of the cell, causing a chain reaction with other cells (especially within the immune and endocrine systems). Mycoplasmas can even cause RNA and DNA mutation of the host cells and have been linked to certain cancers for this reason. Mycoplasmas can also invade and live inside host cells which evade the immune system, especially white blood cells. Once inside a white blood cell, mycoplasmas can travel throughout the body and even cross the blood/brain barrier, and into the central nervous system and spinal fluid.

FOOTNOTES

Baseman, Joel, et.al., Mycoplasmas: Sophisticated, Reemerging, and Burdened by Their Notoriety, CDC, Journal of Infectious Diseases, Vol 3, No.1, Feb 1997

S-C. Mycoplasmas and AIDS. In: Maniloff J, McElhaney RN, Finch LR, Baseman JB, editors. Mycoplasmas: molecular biology and pathogenesis. Washington (DC): American Society for Microbiology, 1992:525-45.

Nicolson G, Nicolson NL. Diagnosis and treatment of mycoplasmal infections in Gulf War illness-CFIDS patients. Intl J Occup Med Immunol Toxicol 1996;5:69-78.

Wear DJ, et.al. Mycoplasmas and oncogenesis:persistent infection and multistage malignant transformation. Proc Natl Acad Sci USA 1995;92:10197-201.

Ekbom A, Daszak P, Kraaz W, Wakefield AJ. Crohn's disease after in-utero measles virus exposure. Lancet 1996;348:516-7.

Taylor-Robinson D. Mycoplasmas in rheumatoid arthritis and other human arthritides. J Clin Pathol 1996;49:781-2.

Dr.Harold Clark, The Intercessor, June 1993, The Road Back Foundation, Delaware OH.

Goulet M, et.al., Isolation of Mycoplasma pneumoniae from the human urogenital tract. J Clin Microbiol 1995;33:2823-5

Daxbock F, et.al., Severe hemolytic anemia and excessive leukocytosis masking mycoplasma pneumonia. Ann Hematol. 2001 Mar;80(3):180-2.

Higuchi ML, et.al., Detection of Mycoplasma pneumoniae and Chlamydia pneumoniae in ruptured atherosclerotic plaques. Braz J Med Biol Res. 2000 Sep;33(9):1023-6.

Socan M, Neurological symptoms in patients whose cerebrospinal fluid is culture- and/or polymerase chain reaction-positive for Mycoplasma pneumoniae. Clin Infect Dis. 2001 Jan 15;32(2):E31-5.

Bencina D, et.al., Intrathecal synthesis of specific antibodies in patients with invasion of the central nervous system by Mycoplasma pneumoniae. Eur J Clin Microbiol Infect Dis. 2000 Jul;19(7):521-30

Smith R, et.al., Neurologic manifestations of Mycoplasma pneumoniae infections: diverse spectrum of diseases. A report of six cases and review of the literature. Clin Pediatr (Phila). 2000 Apr;39(4):195-201.

Umemoto M, Advanced atrioventricular block associated with atrial tachycardia caused by Mycoplasma pneumoniae infection. Acta Paediatr Jpn. 1995 Aug;37(4):518-20.

Lind K. Manifestations and complications of Mycoplasma pneumoniae disease: a review.Yale J Biol Med. 1983 Sep-Dec;56(5-6):461-8.

Alexander FE. Is Mycoplasma Pneumonia associated with childhood acute lymphoblastic leukemia? Cancer Causes Control. 1997 Sep;8(5):803-11.

Hall JE, Mycoplasma pneumonia in acute childhood leukemia. Pediatr Pulmonol. 1985 Nov-Dec;1(6):333-6.

Murphy WH, Gullis C, Dabich L, Heyn R, Zarafonetis CJD. Isolation of Mycoplasma from leukemic and nonleukemia patients. J Nat Cancer Inst 1970;45:243-51.

BACK TO TOP