Mycoplasma infection is respiratory illness caused by Mycoplasma pneumonia, a microscopic organism related to bacteria and fungi. It can be very dangerous. According to Dr. Bill Deagle, over 90% of all biological warfare research conducted in the United States is on mycoplasma, mycotoxins, and nano-bacteria.
Anyone can get the disease, but it most often affects older children and young adults. Children under 5 years usually have mild symptoms or no symptoms at all. The illness is recognized more in school-age children and young adults. Occasionally, epidemics can occur, especially in military populations and institutions (colleges, for example) where people live in close quarters.
Mycoplasma infections occur sporadically throughout the year. Widespread community outbreaks may occur at intervals of four to eight years. Mycoplasma infection is most common in late summer and fall. Mycoplasma is spread through contact with droplets from the nose and throat of infected people especially when they cough and sneeze. Transmission is thought to require prolonged close contact with an infected person. Spread in families, schools and institutions occurs slowly. The contagious period is probably fewer than 10 days and occasionally longer.
Symptoms generally begin 15-25 days after exposure. The symptoms generally develop slowly, over a period of two to four days.Typical symptoms include fever, cough, bronchitis, sore throat, headache and tiredness. A common result of mycoplasma infection is pneumonia (sometimes called “walking pneumonia” because it is usually mild and rarely requires hospitalization). Infections of the middle ear (otitis media) also can result. Symptoms may persist for a few days to more than a month. Mycoplasma can remain in the throat for as long as 13 weeks.
Mycoplasma infection is usually diagnosed on the basis of typical symptoms. A nonspecific blood test (cold agglutinins) is helpful in definitive diagnosis, but is not always positive. The use of more specific laboratory tests is often limited to special outbreak investigations. Many physicians in the US and Canada are untrained thus unskilled in treating this disease. Immunity after mycoplasma infection does occur, but is not lifelong. Second infections are known to occur, although they may be milder. The duration of immunity is unknown.
Antibiotics, antifungals, and diet can be an effective treatment. However, because mycoplasma infection usually resolves on its own, antibiotic treatment of mild symptoms is not always necessary. At this time, there are no vaccines for the prevention of mycoplasma infection and there are no reliably effective measures for control. As with any respiratory disease, all people should cover their face when coughing or sneezing.
Members of the genus Mycoplasma are the smallest organisms lacking cell walls that are capable of self-replication and cause various diseases in humans, animals, and plants. Seven different species of mycoplasma have been associated with various infections in humans. The earliest reports of mycoplasma infectious agents in humans appeared in the 1930s, 1940s and finally, in the early 1960s. The definite relationship between Mycoplasma pneumoniae and the primary atypical pneumoniae was established.
Today, M.pneumoniae remains an important cause of pneumonia and other airway disorders such as tracheobronchitis and pharyngitis. This organism is also associated with extrapulmonary manifestations such as hematopoietic, joint, central nervous system, liver, pancreas and cardiovascular syndromes.
M.genitalium was originally isolated from urethral specimens of two men with nongonococcal urethritis. This organism could be involved in pelvic inflammatory disease. A DNA probe hybridization assay has indicated that M.genitalium was present in urogenital specimens collected from 60% of male homosexual patients with recurrent or persistent nongonococcal urethritis and 22% of heterosexual men with recurrent urethritis, compared with 9% of men without urethritis.
Ureaplasma urealyticum is considered to be a commensal organism in the lower genital tract of sexually-active women and has been found at a colonization rate of 40 to 80%. In some colonized pregnant women, ureaplasmas have been considered to be a cause of chorioamnionitis and premature delivery. They are frequently transmitted from mothers to their infants, and this may cause various diseases which includes pneumonia, persistent pulmonary hypertension, chronic infection of the central nervous system and bronchopulmonary dysplasia.
Mycoplasma fermentans, M. pirum, M. hominis, and M.penetrans
Mycoplasma fermentans, M. pirum, M. hominis, and M. penetrans have been proposed as human pathogens and possible cofactors in HIV infection. These organisms may contribute to the variation in the time from infection with HIV to the development of AIDS symptoms.
Mycoplasma fermentans (incognitus)
Mycoplasma fermentans is considered to be a commensal in the human mucosal tissues and has often been found in saliva and oropharyngeal of 45% of healthy adults. Also, M. fermentans organisms have been isolated from the human urogenital tract and are suspected of invading host tissues from a site of mucosal colonization.
Although mycoplasmas are recognized primarily as extracellular parasites or pathogens of mucosal surfaces, recent evidence suggests that certain species may invade the host cells. The molecular and cellular bases for the invasion of M. fermentans from mucosal cells to the bloodstream and its colonization of blood remain unknown.
Also, it remains unclear whether M. fermentans infection of white blood cells is transient, intermittent or persistent. It is not clear how these stages influence any disease progression. The invasion of host blood cells by M. fermentans is due to inhibition of phagocytosis by a variety of mechanisms, including antiphagocytic proteins such as proteases, phospholipases and by oxygen radicals produced by mycoplasmas.
Mycoplasma fermentans is capable of fusing with lymphocytes and changing their immunological characteristics. Mycoplasma fermentans cells are able to fuse with Tlymphocytes and change their characteristic of cytokine production. By electron microscopy we have been able to show that M. fermentans can indeed fuse with CD4 (Molt-3) cells and induce production of proinflammatory cytokines such as IL-6 and tumor necrosis factor alpha.
Prevalence of M. fermentans in patients with Chronic Fatigue Syndrome (CFS) and comparison with healthy subjects. Using PCR and genetic probes, we were able to demonstrate that between 30 and 35% of CFS patients and 4 to 8% of healthy controls do carry the Mycoplasma fermentans genome in their peripheral blood mononuclear cells. While PCR and genetic probes are rapid and sensitive methods for detecting M. fermentans in clinical specimens, the clinical significance of this organism in Chronic Fatigue Syndrome should be determined by further research studies.
We emphasize that M. fermentans is not the etiologic agent for Chronic Fatigue Syndrome. It may serve as a cofactor in the induction of cytokines and other immune abnormalities found in CFS. These abnormalities may compromise the immune system, allowing other agents, whether they be biological, chemical, or both, to exert an effect resulting in symptomatology shown in CFIDS. Therefore, if the genome of this bacteria is detected in the blood cells of patients with chronic illnesses, treatment with antibiotics may be the logical step for its elimination from the blood.
Mycoplasmafermentans in Persian Gulf War Veterans
Due to the similarity of symptoms in patients of Gulf War Syndrome and Chronic Fatigue Syndrome, experts have applied the PCR and genetic probe methodologies to the blood samples of the soldiers and found a similar percentage (32%) to be positive for the M. fermentans genome. Since the percent detection of M. fermentans genome in Persian Gulf War Syndrome is similar to that of Chronic Fatigue, we believe that M. fermentans is a cofactor and not the major cause of illness in the soldiers of the Persian Gulf War. Mycoplasma, mycotoxins, and depleted uranium (DU) was commonly found.
Claims that HIV genome was inserted in mycoplasma fermentans are unfounded. In one study, it was suggested that pathogenic mycoplasma genomes were genetically manipulated, and part of the HIV genome was inserted into M. fermentans causing a large number of disease cases among veterans. To prove or disprove this claim, we attempted to amplify various regions of the HIV genome by using primers specific for different regions of the HIV genome in the PCR assay. We also utilized the extremely sensitive method of Southern Blot analysis with probes specific for the HIV genome. Using both methodologies we found no portion of the HIV genome among DNA samples of Gulf War veterans who were infected with mycoplasma. In all cases, we found that only the M. fermentans-specific probe reacted with the DNA samples and the specific probe of HIV did not react. The results of this experiment clearly indicate that the above claim regarding insertion of the HIV genome into M. fermentans is scientifically unfounded.
Mycoplasma and Rheumatoid Arthritis
- The occurrence of various mycoplasma and ureaplasma species in joint tissues of patients with rheumatoid arthritis and other human arthritides can no longer be ignored.
- M. fermentans was suggested more than 20 years ago as a cause of rheumatoid arthritis (RA) on the basis of isolation from synovial fluids of a few patients. Recently, with PCR methodology, the M. fermentans genome was found in 40% of synovial biopsy specimens and in 21% of joints of patients with rheumatoid arthritis respectively. This genome was also found in 20% of patients with spondyloarthropathy and psoriatic arthritis and in 13% of patients with unclassified arthritis.
- M. fermentans was not detected in any specimens from patients with reactive arthritis, chronic juvenile arthritis, osteoarthritis or gouty arthritis.
In two recently-published independent randomized trials, rheumatoid arthritis patients were treated with 100 mg of oral minocycline twice daily or a placebo for a period of 26 weeks. In the minocycline group, more minocycline-treated patients than placebo showed greater than 75% improvement in swollen joint count, tender joint count and in clinical parameters such as serum C-reactive protein (CRP) level and erythrocyte sedimentation rate (ESR). In these studies, the intergroup differences were statistically significant for these findings and the mean changes over time revealed continual improvement in the minocycline-treated patients during the entire period of both studies.
This and other presently-available data on minocycline therapy in rheumatoid arthritis suggest that such treatment may be considered along with disease-modifying anti-rheumatic drugs such as methotrexate, sulfasalazine, gold salts and hydroxychloroquine. However, additional clinical research is necessary to document the long-term efficacy of minocycline in the decreased progression of joint destruction. We believe that such long-term study about the efficacy of minocycline should be conducted on patients who are positive for mycoplasma and chlamydia genome (since we detect the chlamydia trachomatis genome in blood and joint fluid of 20% of patients with rheumatoid arthritis) and not by random selection of arthritis patients. Such selection or comparison between mycoplasma- and chlamydia-positive patients with mycoplasma- and chlamydia-negative individuals may further increase the clinical efficacy of minocycline or doxycycline in future double-blind placebo studies.
The eradication of the pathogenic mycoplasmas from blood and various tissue sites requires an intact functional immune system, which most patients with chronic illnesses do not possess. Therefore, immune enhancement strategies along with prolonged drug therapy may help to eliminate mycoplasma from the human body.
Drs. Baseman and Tully, in Emerging Infectious Diseases, Volume3, January-March, 1997, concluded that “the available data and proposed hypotheses that correlate mycoplasmas with disease pathogenesis range from definitive, provocative and titillating to inconclusive, confusing and heretical. Controversy seems to be a recurrent companion of mycoplasmas, yet good science and open-mindedness should overcome the legacy that has burdened them for decades.”
Importance of Measuring IgG and IgM Antibodies Against Mycoplasma Fermentans
We have developed a specific ELISA assay for measurement of antibodies against mycoplasma fermentans and compared the results to the presence of DNA in the blood. We found that only in about 60% of cases where M. fermentans was positive, antibodies to M. fermentans antigens were elevated significantly. In the other 40% in which the genome was positive, IgG and IgM antibodies were not detected. This may be due to the nature of the M. fermentans cell invasion, the inhibition of phagocytosis, and the lack of immune response to this organism in these individuals.
On the contrary, in about 20% of cases, the M. fermentans genome was absent but antibodies of IgG and IgM isotype were detected in their blood.
The absence of M. fermentans DNA from blood cells and the simultaneous presence of antibodies to this mycoplasma in the serum of the same patients suggests chronic infection of other tissues or cells with Mycoplasma fermentans. Another possibility is that these antibodies are cross-reactive in their nature. This means that antibodies produced against collagen, cartilage, and thyroid in some patients with autoimmune disease may cross-react with mycoplasma antigens and give false positive results. For this reason, we measured antibodies against synthesized peptides corresponding to M. fermentans and were able to reduce the degree of cross-reactivity.
Gold standard for detection of mycoplasmas
- The polymerase chain reaction (PCR) for detection of mycoplasma genomes is still the gold standard.
- However, confirmation of PCR should be done by southern blot and molecular probes in order to decrease the rate of false positively and improve false negativity.
- Antibodies (IgG, IgM and IgA) against peptide-specific mycoplasma should be performed simultaneously.
- As no diagnostic tool is 100% accurate, we suggest that PCR, molecular probe, and IgG, IgM, and IgA antibodies should all be performed to gain the most accurate result.